Department Of Microbiology

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Benzotriazole Substituted 2-Phenylquinazolines as Anticancer Agents: Synthesis, Screening, Antiproliferative and Tubulin Polymerization Inhibition Activity
(Bentham Science Publishers, 2022-10-28T00:00:00) Dwivedi, Ashish Ranjan; Rawat, Suraj Singh; Kumar, Vijay; Kumar, Naveen; Kumar, Vinay; Yadav, Ravi Prakash; Baranwal, Somesh; Prasad, Amit; Kumar, Vinod
Aims: Development of anticancer agents targeting tubulin protein. Background: Tubulin protein is being explored as an important target for anticancer drug development. Ligands binding to the colchicine binding site of the tubulin protein act as tubulin polymerization inhibitors and arrest the cell cycle in the G2/M phase. Objective: Synthesis and screening of benzotriazole-substituted 2-phenyl quinazolines as potential anticancer agents. Methods: A series of benzotriazole-substituted quinazoline derivatives have been synthesized and evaluated against human MCF-7 (breast), HeLa (cervical) and HT-29 (colon) cancer cell lines using standard MTT assays. Results: ARV-2 with IC50 values of 3.16 �M, 5.31 �M, 10.6 �M against MCF-7, HELA and HT29 cell lines, respectively displayed the most potent antiproliferative activities in the series while all the compounds were found non-toxic against HEK293 (normal cells). In the mechanistic studies involving cell cycle analysis, apoptosis assay and JC-1 studies, ARV-2 and ARV-3 were found to induce mitochondria-mediated apoptosis. Conclusion: The benzotriazole-substituted 2-phenyl quinazolines have the potential to be developed as potent anticancer agents. � 2023 Bentham Science Publishers.
Benzotriazole Substituted 2-Phenylquinazolines as Anticancer Agents: Synthesis, Screening, Antiproliferative and Tubulin Polymerization Inhibition Activity
(Bentham Science Publishers, 2022-10-28T00:00:00) Dwivedi, Ashish Ranjan; Rawat, Suraj Singh; Kumar, Vijay; Kumar, Naveen; Kumar, Vinay; Yadav, Ravi Prakash; Baranwal, Somesh; Prasad, Amit; Kumar, Vinod
Aims: Development of anticancer agents targeting tubulin protein. Background: Tubulin protein is being explored as an important target for anticancer drug development. Ligands binding to the colchicine binding site of the tubulin protein act as tubulin polymerization inhibitors and arrest the cell cycle in the G2/M phase. Objective: Synthesis and screening of benzotriazole-substituted 2-phenyl quinazolines as potential anticancer agents. Methods: A series of benzotriazole-substituted quinazoline derivatives have been synthesized and evaluated against human MCF-7 (breast), HeLa (cervical) and HT-29 (colon) cancer cell lines using standard MTT assays. Results: ARV-2 with IC50 values of 3.16 �M, 5.31 �M, 10.6 �M against MCF-7, HELA and HT29 cell lines, respectively displayed the most potent antiproliferative activities in the series while all the compounds were found non-toxic against HEK293 (normal cells). In the mechanistic studies involving cell cycle analysis, apoptosis assay and JC-1 studies, ARV-2 and ARV-3 were found to induce mitochondria-mediated apoptosis. Conclusion: The benzotriazole-substituted 2-phenyl quinazolines have the potential to be developed as potent anticancer agents. � 2023 Bentham Science Publishers.
Brain Exosomes: Friend or Foe in Alzheimer�s Disease?
(Springer, 2021-09-30T00:00:00) Kaur, Sharanjot; Verma, Harkomal; Dhiman, Monisha; Tell, Gianluca; Gigli, Gian Luigi; Janes, Francesco; Mantha, Anil K.
Alzheimer�s disease (AD) is the most common neurodegenerative disease. It is known to be a multifactorial disease and several causes are associated with its occurrence as well as progression. However, the accumulation of amyloid beta (A?) is widely considered its major pathogenic hallmark. Additionally, neurofibrillary tangles (NFT), mitochondrial dysfunction, oxidative stress, and aging (cellular senescence) are considered as additional hits affecting the disease pathology. Several studies are now suggesting important role of inflammation in AD, which shifts our thought towards the brain�s resident immune cells, microglia, and astrocytes; how they interact with neurons; and how these interactions are affected by intra and extracellular stressful factors. These interactions can be modulated by different mechanisms and pathways, in which exosomes could play an important role. Exosomes are multivesicular bodies secreted by nearly all types of cells. The exosomes secreted by glial cells or neurons affect the interactions and thus the physiology of these cells by transmitting miRNAs, proteins, and lipids. Exosomes can serve as a friend or foe to the neuron function, depending upon the carried signals. Exosomes, from the healthy microenvironment, may assist neuron function and health, whereas, from the stressed microenvironment, they carry oxidative and inflammatory signals to the neurons and thus prove detrimental to the neuronal function. Furthermore, exosomes can cross the blood�brain barrier (BBB), and from the blood plasma they can enter the brain cells and activate microglia and astrocytes. Exosomes can transport A? or Tau, cytokines, miRNAs between the cells, and alter the physiology of recipient cells. They can also assist in A? clearance and regulation of synaptic activity. The exosomes derived from different cells play different roles, and this field is still in its infancy stage. This review advocates exosomes� role as a friend or foe in neurodegenerative diseases, especially in the case of Alzheimer�s disease. � 2021, The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.
Brain Exosomes: Friend or Foe in Alzheimer�s Disease?
(Springer, 2021-09-30T00:00:00) Kaur, Sharanjot; Verma, Harkomal; Dhiman, Monisha; Tell, Gianluca; Gigli, Gian Luigi; Janes, Francesco; Mantha, Anil K.
Alzheimer�s disease (AD) is the most common neurodegenerative disease. It is known to be a multifactorial disease and several causes are associated with its occurrence as well as progression. However, the accumulation of amyloid beta (A?) is widely considered its major pathogenic hallmark. Additionally, neurofibrillary tangles (NFT), mitochondrial dysfunction, oxidative stress, and aging (cellular senescence) are considered as additional hits affecting the disease pathology. Several studies are now suggesting important role of inflammation in AD, which shifts our thought towards the brain�s resident immune cells, microglia, and astrocytes; how they interact with neurons; and how these interactions are affected by intra and extracellular stressful factors. These interactions can be modulated by different mechanisms and pathways, in which exosomes could play an important role. Exosomes are multivesicular bodies secreted by nearly all types of cells. The exosomes secreted by glial cells or neurons affect the interactions and thus the physiology of these cells by transmitting miRNAs, proteins, and lipids. Exosomes can serve as a friend or foe to the neuron function, depending upon the carried signals. Exosomes, from the healthy microenvironment, may assist neuron function and health, whereas, from the stressed microenvironment, they carry oxidative and inflammatory signals to the neurons and thus prove detrimental to the neuronal function. Furthermore, exosomes can cross the blood�brain barrier (BBB), and from the blood plasma they can enter the brain cells and activate microglia and astrocytes. Exosomes can transport A? or Tau, cytokines, miRNAs between the cells, and alter the physiology of recipient cells. They can also assist in A? clearance and regulation of synaptic activity. The exosomes derived from different cells play different roles, and this field is still in its infancy stage. This review advocates exosomes� role as a friend or foe in neurodegenerative diseases, especially in the case of Alzheimer�s disease. � 2021, The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.
Burden of dengue, leishmaniasis and lymphatic filariasis in India and its states from 1990�2019: Analysis from the Global Burden of Disease study (GBD 2019)
(Public Library of Science, 2023-10-18T00:00:00) Dutta, Omprokash; Prasanth, Ajay; Kumari, Ashu; Akanksha, Kumari; Deeba, Farah; Salam, Nasir
Vector-borne diseases such as dengue, leishmaniasis, and lymphatic filariasis, constitute significant sources of illness, disability, and mortality among the poor and vulnerable in many countries around the world, including India. Based on the global burden of diseases, injuries, and risk factors study 2019, we analyse the burden of dengue, leishmaniasis, and lymphatic filariasis, in India from 1990 to 2019. Over this period, there was a reduction in the burden of lymphatic filariasis and leishmaniasis. Notably, dengue emerged as the most common vector-borne disease, exhibiting high fatality rate above 15 years of age and the highest DALY within 15�49 age group. Additionally, dengue cases surged substantially between 1990 and 2019. Leishmaniasis related mortality and DALY declined in the year 2019 compared to the year 1990, with high mortality and DALY in the 0-49-year-old age group. For lymphatic filariasis, DALY was more pronounce among those in the 15�49-year age group, which underwent reduction in 2019. Males had a higher burden in other vector-borne diseases than females, although females had a slightly elevated dengue burden. These findings highlight the evolving epidemiological trends related to vector-borne diseases in India, over the last three decades and underline the critical significance of sustained efforts for the elimination and control of vector-borne diseases. � 2023 Dutta et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Burden of dengue, leishmaniasis and lymphatic filariasis in India and its states from 1990�2019: Analysis from the Global Burden of Disease study (GBD 2019)
(Public Library of Science, 2023-10-18T00:00:00) Dutta, Omprokash; Prasanth, Ajay; Kumari, Ashu; Akanksha, Kumari; Deeba, Farah; Salam, Nasir
Vector-borne diseases such as dengue, leishmaniasis, and lymphatic filariasis, constitute significant sources of illness, disability, and mortality among the poor and vulnerable in many countries around the world, including India. Based on the global burden of diseases, injuries, and risk factors study 2019, we analyse the burden of dengue, leishmaniasis, and lymphatic filariasis, in India from 1990 to 2019. Over this period, there was a reduction in the burden of lymphatic filariasis and leishmaniasis. Notably, dengue emerged as the most common vector-borne disease, exhibiting high fatality rate above 15 years of age and the highest DALY within 15�49 age group. Additionally, dengue cases surged substantially between 1990 and 2019. Leishmaniasis related mortality and DALY declined in the year 2019 compared to the year 1990, with high mortality and DALY in the 0-49-year-old age group. For lymphatic filariasis, DALY was more pronounce among those in the 15�49-year age group, which underwent reduction in 2019. Males had a higher burden in other vector-borne diseases than females, although females had a slightly elevated dengue burden. These findings highlight the evolving epidemiological trends related to vector-borne diseases in India, over the last three decades and underline the critical significance of sustained efforts for the elimination and control of vector-borne diseases. � 2023 Dutta et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Colistin Resistance and Management of Drug Resistant Infections
(Hindawi Limited, 2022-12-10T00:00:00) Sharma, Juhi; Sharma, Divakar; Singh, Amit; Sunita, Kumari
Colistin resistance is a globalized sensible issue because it has been considered a drug of the last-line resort to treat drug-resistant bacterial infections. The product of the mobilized colistin resistance (mcr) gene and its variants are the significant causes of colistin resistance, which is emerging due to the frequent colistin use in veterinary, and these genes circulate among the bacterial community. Apart from mcr genes, some other intrinsic genes and proteins are also involved in colistin resistance. Researchers focus on the most advanced genomics (whole genome sequencing), proteomics, and bioinformatics approaches to explore the question of colistin resistance. To combat colistin resistance, researchers developed various strategies such as the development of newer drugs, the repurposing of existing drugs, combinatorial treatment by colistin with other drugs, a nano-based approach, photodynamic therapy, a CRISPRi-based strategy, and a phage-based strategy. In this timeline review, we have discussed the development of colistin resistance and its management in developing countries. � 2022 Juhi Sharma et al.
Colistin Resistance and Management of Drug Resistant Infections
(Hindawi Limited, 2022-12-10T00:00:00) Sharma, Juhi; Sharma, Divakar; Singh, Amit; Sunita, Kumari
Colistin resistance is a globalized sensible issue because it has been considered a drug of the last-line resort to treat drug-resistant bacterial infections. The product of the mobilized colistin resistance (mcr) gene and its variants are the significant causes of colistin resistance, which is emerging due to the frequent colistin use in veterinary, and these genes circulate among the bacterial community. Apart from mcr genes, some other intrinsic genes and proteins are also involved in colistin resistance. Researchers focus on the most advanced genomics (whole genome sequencing), proteomics, and bioinformatics approaches to explore the question of colistin resistance. To combat colistin resistance, researchers developed various strategies such as the development of newer drugs, the repurposing of existing drugs, combinatorial treatment by colistin with other drugs, a nano-based approach, photodynamic therapy, a CRISPRi-based strategy, and a phage-based strategy. In this timeline review, we have discussed the development of colistin resistance and its management in developing countries. � 2022 Juhi Sharma et al.
Correlative study on heavy metal-induced oxidative stress and hypertension among the rural population of Malwa Region of Punjab, India
(Springer Science and Business Media Deutschland GmbH, 2022-07-26T00:00:00) Kaur, Sukhchain; Garg, Neha; Rubal, Rubal; Dhiman, Monisha
Heavy metal-induced toxicity contributes to the progression of various metabolic disorders and possible mechanisms involved in disease progression are not well established. In this study, the correlation of heavy metal exposure and hypertension have been demonstrated. The results showed that in hypertensive subjects, the lipid profiles (triglycerides, LDL-C, HDL-C, and total cholesterol) and cardiac markers (CK-MB and LDH) were altered abruptly. As a consequence of heavy- induced oxidative stress, the oxidants (TBARS and protein carbonyls) and antioxidants (SOD, GSH, and TAC) were significantly increased and decreased, respectively in hypertension�subjects. The concentrations of heavy metals (Pb, Cd, and As) exceeded the permissible limits in hypertensive subjects. The Nrf-2 genotyping indicated that heavy metals may induce mutations at molecular level. The results of correlation analysis revealed that�the heavy metals interact with cellular components and interfere with metabolic processes which then�results in disturbed lipid profile, enhanced oxidative stress, and reduced antioxidant status. The current study systematically estimated the association of hair and nail heavy metal concentrations with hypertension among the population residing in the Malwa region of Punjab. The proposed study highlighted that heavy metals act as a silent risk factor in the hypertension progression in the population of Malwa region. Future studies are required to confirm current findings and further scrutinize the effect of heavy metals exposure in early adulthood, early, and late mid-life to develop metabolic complications such as hypertension. � 2022, The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.
Correlative study on heavy metal-induced oxidative stress and hypertension among the rural population of Malwa Region of Punjab, India
(Springer Science and Business Media Deutschland GmbH, 2022-07-26T00:00:00) Kaur, Sukhchain; Garg, Neha; Rubal, Rubal; Dhiman, Monisha
Heavy metal-induced toxicity contributes to the progression of various metabolic disorders and possible mechanisms involved in disease progression are not well established. In this study, the correlation of heavy metal exposure and hypertension have been demonstrated. The results showed that in hypertensive subjects, the lipid profiles (triglycerides, LDL-C, HDL-C, and total cholesterol) and cardiac markers (CK-MB and LDH) were altered abruptly. As a consequence of heavy- induced oxidative stress, the oxidants (TBARS and protein carbonyls) and antioxidants (SOD, GSH, and TAC) were significantly increased and decreased, respectively in hypertension�subjects. The concentrations of heavy metals (Pb, Cd, and As) exceeded the permissible limits in hypertensive subjects. The Nrf-2 genotyping indicated that heavy metals may induce mutations at molecular level. The results of correlation analysis revealed that�the heavy metals interact with cellular components and interfere with metabolic processes which then�results in disturbed lipid profile, enhanced oxidative stress, and reduced antioxidant status. The current study systematically estimated the association of hair and nail heavy metal concentrations with hypertension among the population residing in the Malwa region of Punjab. The proposed study highlighted that heavy metals act as a silent risk factor in the hypertension progression in the population of Malwa region. Future studies are required to confirm current findings and further scrutinize the effect of heavy metals exposure in early adulthood, early, and late mid-life to develop metabolic complications such as hypertension. � 2022, The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.
Cyanobacteria-mediated heavy metal and xenobiotic bioremediation
(Springer Nature, 2023-06-24T00:00:00) Lalrokimi, X.; Mehetre, Gajanan; Zothanpuia, X.; Singh, Bhim Pratap; Yadav, Mukesh Kumar; Lalnunmawii, Esther
Overpopulation and industrialization are the leading cause of environmental pollution. However, environmental pollutants such as xenobiotics and heavy metals are of more concern because of their toxicity; in addition, the degradation of both compounds is impossible and persists in the environment for a longer time. Photoautotrophic microorganism such as cyanobacteria is considered to be the potential organism in the process of bioremediation because of its ability to photosynthetically break down toxic heavy metals and xenobiotic compounds into less toxic forms. It is also known to be conventional, eco-friendly, and cost-effective. This chapter highlighted the capability of different genera of cyanobacteria in the biodegradation of heavy metals and xenobiotics. � The Author(s), under exclusive license to Springer Nature Singapore Pte Ltd. 2023.
Cyanobacteria-mediated heavy metal and xenobiotic bioremediation
(Springer Nature, 2023-06-24T00:00:00) Lalrokimi, X.; Mehetre, Gajanan; Zothanpuia, X.; Singh, Bhim Pratap; Yadav, Mukesh Kumar; Lalnunmawii, Esther
Overpopulation and industrialization are the leading cause of environmental pollution. However, environmental pollutants such as xenobiotics and heavy metals are of more concern because of their toxicity; in addition, the degradation of both compounds is impossible and persists in the environment for a longer time. Photoautotrophic microorganism such as cyanobacteria is considered to be the potential organism in the process of bioremediation because of its ability to photosynthetically break down toxic heavy metals and xenobiotic compounds into less toxic forms. It is also known to be conventional, eco-friendly, and cost-effective. This chapter highlighted the capability of different genera of cyanobacteria in the biodegradation of heavy metals and xenobiotics. � The Author(s), under exclusive license to Springer Nature Singapore Pte Ltd. 2023.
Gliadin induced oxidative stress and altered cellular responses in human intestinal cells: An in-vitro study to understand the cross-talk between the transcription factor Nrf-2 and multifunctional APE1 enzyme
(John Wiley and Sons Inc, 2022-05-09T00:00:00) Gupta, Kunj Bihari; Dhiman, Monisha; Mantha, Anil Kumar
The present study examined the wheat protein gliadin-induced oxidative and nitrosative stress and its downstream responses in human intestinal HCT-116 and HT-29 cells. The beneficial role of dietary phytochemical curcumin and role of multifunctional enzyme Apurinic/aprymidinic endonuclease 1 (APE1) a major player involved in the base excision repair (BER)-pathway in gliadin intolerant intestinal HCT-116 and HT-29 cell lines were evaluated as an in vitro model study. The cultured cells were exposed to gliadin protein, H2O2, and curcumin followed by the assessment of oxidative stress and the consequences were measured using spectrophotometric, PCR, flow cytometer, Western blotting, confocal microscopy, and other methods. Results demonstrate that a 3 h pretreatment of curcumin, followed by the treatment of gliadin protein for 24 h time period protected both the HCT-116 and HT-29 cells via: (i) decreasing the ROS/RNS, restoring the mitochondrial transmembrane potential; (ii) re-establishing the cellular antioxidant defense system (superoxide dismutase, catalase, and GSH); (iii) enhancing the functions of APE1 viz. endonuclease activity and redox activation of transcription factor Nrf-2, the later binds with the antioxidant response elements (ARE) and activates downstream targets involved in cell survival. The cross-talk between APE1 and Nrf-2 was also established using immunofluorescence imaging and co-immunoprecipitation assays. In conclusion, gliadin protein induces oxidative/nitrosative stress, mitochondrial dysfunction and it damages cellular biomolecules in the intestinal cells. Hence it can be attributed to the tissue damage and disease pathogenesis in wheat intolerance-associated intestinal diseases. The gliadin-induced stress and its consequences are significantly reduced by the pretreatment of curcumin via BER-pathway and ARE-pathway; which is evident through the interaction between these two essential proteins. Hence suggesting for the intervention of curcumin and other natural dietary phytochemicals-based disease management and treatment of gliadin intolerance associated intestinal diseases like celiac disease. � 2022 Wiley Periodicals LLC.
Gliadin induced oxidative stress and altered cellular responses in human intestinal cells: An in-vitro study to understand the cross-talk between the transcription factor Nrf-2 and multifunctional APE1 enzyme
(John Wiley and Sons Inc, 2022-05-09T00:00:00) Gupta, Kunj Bihari; Dhiman, Monisha; Mantha, Anil Kumar
The present study examined the wheat protein gliadin-induced oxidative and nitrosative stress and its downstream responses in human intestinal HCT-116 and HT-29 cells. The beneficial role of dietary phytochemical curcumin and role of multifunctional enzyme Apurinic/aprymidinic endonuclease 1 (APE1) a major player involved in the base excision repair (BER)-pathway in gliadin intolerant intestinal HCT-116 and HT-29 cell lines were evaluated as an in vitro model study. The cultured cells were exposed to gliadin protein, H2O2, and curcumin followed by the assessment of oxidative stress and the consequences were measured using spectrophotometric, PCR, flow cytometer, Western blotting, confocal microscopy, and other methods. Results demonstrate that a 3 h pretreatment of curcumin, followed by the treatment of gliadin protein for 24 h time period protected both the HCT-116 and HT-29 cells via: (i) decreasing the ROS/RNS, restoring the mitochondrial transmembrane potential; (ii) re-establishing the cellular antioxidant defense system (superoxide dismutase, catalase, and GSH); (iii) enhancing the functions of APE1 viz. endonuclease activity and redox activation of transcription factor Nrf-2, the later binds with the antioxidant response elements (ARE) and activates downstream targets involved in cell survival. The cross-talk between APE1 and Nrf-2 was also established using immunofluorescence imaging and co-immunoprecipitation assays. In conclusion, gliadin protein induces oxidative/nitrosative stress, mitochondrial dysfunction and it damages cellular biomolecules in the intestinal cells. Hence it can be attributed to the tissue damage and disease pathogenesis in wheat intolerance-associated intestinal diseases. The gliadin-induced stress and its consequences are significantly reduced by the pretreatment of curcumin via BER-pathway and ARE-pathway; which is evident through the interaction between these two essential proteins. Hence suggesting for the intervention of curcumin and other natural dietary phytochemicals-based disease management and treatment of gliadin intolerance associated intestinal diseases like celiac disease. � 2022 Wiley Periodicals LLC.
Global, regional, and national sex differences in the global burden of tuberculosis by HIV status, 1990�2019: results from the Global Burden of Disease Study 2019
(Elsevier Ltd, 2021-09-23T00:00:00) Ledesma, Jorge R.; Ma, Jianing; Vongpradith, Avina; Maddison, Emilie R.; Novotney, Amanda; Biehl, Molly H.; Legrand, Kate E.; Ross, Jennifer M.; Jahagirdar, Deepa; Bryazka, Dana; Feldman, Rachel; Abolhassani, Hassan; Abosetugn, Akine Eshete; Abu-Gharbieh, Eman; Adebayo, Oladimeji M.; Adnani, Qorinah Estiningtyas Sakilah; Afzal, Saira; Ahinkorah, Bright Opoku; Ahmad, Sajjad Ahmad; Ahmadi, Sepideh; Rashid, Tarik Ahmed; Salih, Yusra Ahmed; Aklilu, Addis; Akunna, Chisom Joyqueenet; Al Hamad, Hanadi; Alahdab, Fares; Alemayehu, Yosef; Alene, Kefyalew Addis; Ali, Beriwan Abdulqadir; Ali, Liaqat; Alipour, Vahid; Alizade, Hesam; Al-Raddadi, Rajaa M.; Alvis-Guzman, Nelson; Amini, Saeed; Amit, Arianna Maever L.; Anderson, Jason A.; Androudi, Sofa; Antonio, Carl Abelardo T.; Antony, Catherine M.; Anwer, Razique; Arabloo, Jalal; Arja, Asrat; Asemahagn, Mulusew A.; Atre, Sachin R.; Azhar, Gulrez Shah; Darshan, B.B.; Babar, Zaheer-Ud-Din; Baig, Atif Amin; Banach, Maciej; Barqawi, Hiba Jawdat; Barra, Fabio; Barrow, Amadou; Basu, Sanjay; Belgaumi, Uzma Iqbal; Bhagavathula, Akshaya Srikanth; Bhardwaj, Nikha; Bhardwaj, Pankaj; Bhattacharjee, Natalia V.; Bhattacharyya, Krittika; Bijani, Ali; Bikbov, Boris; Boloor, Archith; Briko, Nikolay Ivanovich; Buonsenso, Danilo; Nagaraja, Sharath Burugina; Butt, Zahid A.; Carter, Austin; Carvalho, Felix; Charan, Jaykaran; Chatterjee, Souranshu; Chattu, Soosanna Kumary; Chattu, Vijay Kumar; Christopher, Devasahayam J.; Chu, Dinh-Toi; Claassens, Mareli M.; Dadras, Omid; Dagnew, Amare Belachew; Dai, Xiaochen; Dandona, Lalit; Dandona, Rakhi; Daneshpajouhnejad, Parnaz; Darwesh, Aso Mohammad; Dhamnetiya, Deepak; Dianatinasab, Mostafa; Diaz, Daniel; Doan, Linh Phuong; Eftekharzadeh, Sahar; Elhadi, Muhammed; Emami, Amir; Enany, Shymaa; Faraon, Emerito Jose A.; Farzadfar, Farshad; Fernandes, Eduarda; Desideri, Lorenzo Ferro; Filip, Irina; Fischer, Florian; Foroutan, Masoud; Frank, Tahvi D.; Garcia-Basteiro, Alberto L.; Garcia-Calavaro, Christian; Garg, Tushar; Geberemariyam, Biniyam Sahiledengle; Ghadiri, Keyghobad; Ghashghaee, Ahmad; Golechha, Mahaveer; Goodridge, Amador; Gupta, Bhawna; Gupta, Sapna; Gupta, Veer Bala; Gupta, Vivek Kumar; Haider, Mohammad Rifat; Hamidi, Samer; Hanif, Asif; Haque, Shaful; Harapan, Harapan; Hargono, Arief; Hasaballah, Ahmed I.; Hashi, Abdiwahab; Hassan, Shoaib; Hassankhani, Hadi; Hayat, Khezar; Hezam, Kamal; Holla, Ramesh; Hosseinzadeh, Mehdi; Hostiuc, Mihaela; Househ, Mowafa; Hussain, Rabia; Ibitoye, Segun Emmanuel; Ilic, Irena M.; Ilic, Milena D.; Irvani, Seyed Sina Naghibi; Ismail, Nahlah Elkudssiah; Itumalla, Ramaiah; Jaafari, Jalil; Jacobsen, Kathryn H.; Jain, Vardhmaan; Javanmardi, Fatemeh; Jayapal, Sathish Kumar; Jayaram, Shubha; Jha, Ravi Prakash; Jonas, Jost B.; Joseph, Nitin; Joukar, Farahnaz; Kabir, Zubair; Kamath, Ashwin; Kanchan, Tanuj; Kandel, Himal; Katoto, Patrick D.M.C.; Kayode, Gbenga A.; Kendrick, Parkes J.; Kerbo, Amene Abebe; Khajuria, Himanshu; Khalilov, Rovshan; Khatab, Khaled; Khoja, Abdullah T.; Khubchandani, Jagdish; Kim, Min Seo; Kim, Yun Jin; Kisa, Adnan; Kisa, Sezer; Kosen, Soewarta; Koul, Parvaiz A.; Laxminarayana, Sindhura Lakshmi Koulmane; Koyanagi, Ai; Krishan, Kewal; Bicer, Burcu Kucuk; Kumar, Avinash; Kumar, G. Anil; Kumar, Narinder; Kumar, Nithin; Kwarteng, Alexander; Lak, Hassan Mehmood; Lal, Dharmesh Kumar; Landires, Iv�n; Lasrado, Savita; Lee, Shaun Wen Huey; Lee, Wei-Chen; Lin, Christine; Liu, Xuefeng; Lopukhov, Platon D.; Lozano, Rafael; Machado, Daiane Borges; Kunjathur, Shilpashree Madhava; Madi, Deepak; Mahajan, Preetam Bhalchandra; Majeed, Azeem; Malik, Ahmad Azam; Martins-Melo, Francisco Rogerl�ndio; Mehta, Saurabh; Memish, Ziad A.; Mendoza, Walter; Menezes, Ritesh G.; Merie, Hayimro Edemealem; Mersha, Amanual Getnet; Mesregah, Mohamed Kamal; Mestrovic, Tomislav; Mheidly, Nour Mheidly; Misra, Sanjeev; Mithra, Prasanna; Moghadaszadeh, Masoud; Mohammadi, Mokhtar; Mohammadian-Hafshejani, Abdollah; Mohammed, Shafu; Molokhia, Mariam; Moni, Mohammad Ali; Al Montasir, Ahmed; Moore, Catrin E.; Nagarajan, Ahamarshan Jayaraman; Nair, Sanjeev; Nair, Suma; Naqvi, Atta Abbas; Swamy, Sreenivas Narasimha; Nayak, Biswa Prakash; Nazari, Javad; Kandel, Sandhya Neupane; Nguyen, Trang Huyen; Nixon, Molly R.; Nnaji, Chukwudi A.; Ntsekhe, Mpiko; Nu�ez-Samudio, Virginia; Oancea, Bogdan; Odukoya, Oluwakemi Ololade; Olagunju, Andrew T.; Oren, Eyal; Mahesh, P.A.; Parthasarathi, Ramakrishnan; Kan, Fatemeh Pashazadeh; Pattanshetty, Sanjay M.; Paudel, Rajan; Paul, Pintu; Pawar, Shrikant; Pepito, Veincent Christian Filipino; Perico, Norberto; Pirestani, Majid; Polibin, Roman V.; Postma, Maarten J.; Pourshams, Akram; Prashant, Akila; Pribadi, Dimas Ria Angga; Radfar, Amir; Rafei, Alireza; Rahim, Fakher; Rahimi-Movaghar, Vafa; Rahman, Mahfuzar; Rahman, Mosiur; Rahmani, Amir Masoud; Ranasinghe, Priyanga; Rao, Chythra R.; Rawaf, David Laith; Rawaf, Salman; Reitsma, Marissa B.; Remuzzi, Giuseppe; Renzaho, Andre M. N.; Reta, Melese Abate; Rezaei, Nima; Rezahosseini, Omid; Rezai, Mohammad Sadegh; Rezapour, Aziz; Roshandel, Gholamreza; Roshchin, Denis O.; Sabour, Siamak; Saif-Ur-rahman, K.M.; Salam, Nasir; Kafl, Hossein Samadi; Samaei, Mehrnoosh; Samy, Abdallah M.; Saroshe, Satish; Sartorius, Benn; Sathian, Brijesh; Sawyer, Susan M.; Senthilkumaran, Subramanian; Seylani, Allen; Shafaat, Omid; Shaikh, Masood Ali; Sharaf, Kiomars; Shetty, Ranjitha S.; Shigematsu, Mika; Shin, Jae Il; Silva, Jo�o Pedro; Singh, Jitendra Kumar; Sinha, Smriti; Skryabin, Valentin Yurievich; Skryabina, Anna Aleksandrovna; Spurlock, Emma Elizabeth; Sreeramareddy, Chandrashekhar T.; Steiropoulos, Paschalis; Sufyan, Mu'awiyyah Babale; Tabuchi, Takahiro; Tadesse, Eyayou Girma; Tamir, Zemenu; Tarkang, Elvis Enowbeyang; Tekalegn, Yohannes; Tesfay, Fisaha Haile; Tessema, Belay; Thapar, Rekha; Tleyjeh, Imad I.; Tobe-Gai, Ruoyan; Tran, Bach Xuan; Tsegaye, Berhan; Tsegaye, Gebiyaw Wudie; Ullah, Anayat; Umeokonkwo, Chukwuma David; Tahbaz, Sahel Valadan; Vo, Bay; Vu, Giang Thu; Waheed, Yasir; Walters, Magdalene K.; Whisnant, Joanna L.; Woldekidan, Mesfn Agachew; Wubishet, Befkadu Legesse; Jabbari, Seyed Hossein Yahyazadeh; Yazie, Taklo Simeneh Yazie; Yeshaw, Yigizie; Yi, Siyan; Yigit, Vahit; Yonemoto, Naohiro; Yu, Chuanhua; Yunusa, Ismaeel; Zastrozhin, Mikhail Sergeevich; Zastrozhina, Anasthasia; Zhang, Zhi-Jiang; Zumla, Alimuddin; Mokdad, Ali H.; Salomon, Joshua A.; Reiner, Robert C.; Lim, Stephen S.; Naghavi, Mohsen; Vos, Theo; Hay, Simon I.; Murray, Christopher J. L.; Kyu, Hmwe Hmwe
Background: Tuberculosis is a major contributor to the global burden of disease, causing more than a million deaths annually. Given an emphasis on equity in access to diagnosis and treatment of tuberculosis in global health targets, evaluations of differences in tuberculosis burden by sex are crucial. We aimed to assess the levels and trends of the global burden of tuberculosis, with an emphasis on investigating differences in sex by HIV status for 204 countries and territories from 1990 to 2019. Methods: We used a Bayesian hierarchical Cause of Death Ensemble model (CODEm) platform to analyse 21 505 site-years of vital registration data, 705 site-years of verbal autopsy data, 825 site-years of sample-based vital registration data, and 680 site-years of mortality surveillance data to estimate mortality due to tuberculosis among HIV-negative individuals. We used a population attributable fraction approach to estimate mortality related to HIV and tuberculosis coinfection. A compartmental meta-regression tool (DisMod-MR 2.1) was then used to synthesise all available data sources, including prevalence surveys, annual case notifications, population-based tuberculin surveys, and tuberculosis cause-specific mortality, to produce estimates of incidence, prevalence, and mortality that were internally consistent. We further estimated the fraction of tuberculosis mortality that is attributable to independent effects of risk factors, including smoking, alcohol use, and diabetes, for HIV-negative individuals. For individuals with HIV and tuberculosis coinfection, we assessed mortality attributable to HIV risk factors including unsafe sex, intimate partner violence (only estimated among females), and injection drug use. We present 95% uncertainty intervals for all estimates. Findings: Globally, in 2019, among HIV-negative individuals, there were 1�18 million (95% uncertainty interval 1�08�1�29) deaths due to tuberculosis and 8�50 million (7�45�9�73) incident cases of tuberculosis. Among HIV-positive individuals, there were 217 000 (153 000�279 000) deaths due to tuberculosis and 1�15 million (1�01�1�32) incident cases in 2019. More deaths and incident cases occurred in males than in females among HIV-negative individuals globally in 2019, with 342 000 (234 000�425 000) more deaths and 1�01 million (0�82�1�23) more incident cases in males than in females. Among HIV-positive individuals, 6250 (1820�11 400) more deaths and 81 100 (63 300�100 000) more incident cases occurred among females than among males in 2019. Age-standardised mortality rates among HIV-negative males were more than two times greater in 105 countries and age-standardised incidence rates were more than 1�5 times greater in 74 countries than among HIV-negative females in 2019. The fraction of global tuberculosis deaths among HIV-negative individuals attributable to alcohol use, smoking, and diabetes was 4�27 (3�69�5�02), 6�17 (5�48�7�02), and 1�17 (1�07�1�28) times higher, respectively, among males than among females in 2019. Among individuals with HIV and tuberculosis coinfection, the fraction of mortality attributable to injection drug use was 2�23 (2�03�2�44) times greater among males than females, whereas the fraction due to unsafe sex was 1�06 (1�05�1�08) times greater among females than males. Interpretation: As countries refine national tuberculosis programmes and strategies to end the tuberculosis epidemic, the excess burden experienced by males is important. Interventions are needed to actively communicate, especially to men, the importance of early diagnosis and treatment. These interventions should occur in parallel with efforts to minimise excess HIV burden among women in the highest HIV burden countries that are contributing to excess HIV and tuberculosis coinfection burden for females. Placing a focus on tuberculosis burden among HIV-negative males and HIV and tuberculosis coinfection among females might help to diminish the overall burden of tuberculosis. This strategy will be crucial in reaching both equity and burden targets outlined by global health milestones. Funding: Bill & Melinda Gates Foundation. � 2022 The Author(s). Published by Elsevier Ltd. This is an Open Access article under the CC BY 4.0 license
Global, regional, and national sex differences in the global burden of tuberculosis by HIV status, 1990�2019: results from the Global Burden of Disease Study 2019
(Elsevier Ltd, 2021-09-23T00:00:00) Ledesma, Jorge R.; Ma, Jianing; Vongpradith, Avina; Maddison, Emilie R.; Novotney, Amanda; Biehl, Molly H.; Legrand, Kate E.; Ross, Jennifer M.; Jahagirdar, Deepa; Bryazka, Dana; Feldman, Rachel; Abolhassani, Hassan; Abosetugn, Akine Eshete; Abu-Gharbieh, Eman; Adebayo, Oladimeji M.; Adnani, Qorinah Estiningtyas Sakilah; Afzal, Saira; Ahinkorah, Bright Opoku; Ahmad, Sajjad Ahmad; Ahmadi, Sepideh; Rashid, Tarik Ahmed; Salih, Yusra Ahmed; Aklilu, Addis; Akunna, Chisom Joyqueenet; Al Hamad, Hanadi; Alahdab, Fares; Alemayehu, Yosef; Alene, Kefyalew Addis; Ali, Beriwan Abdulqadir; Ali, Liaqat; Alipour, Vahid; Alizade, Hesam; Al-Raddadi, Rajaa M.; Alvis-Guzman, Nelson; Amini, Saeed; Amit, Arianna Maever L.; Anderson, Jason A.; Androudi, Sofa; Antonio, Carl Abelardo T.; Antony, Catherine M.; Anwer, Razique; Arabloo, Jalal; Arja, Asrat; Asemahagn, Mulusew A.; Atre, Sachin R.; Azhar, Gulrez Shah; Darshan, B.B.; Babar, Zaheer-Ud-Din; Baig, Atif Amin; Banach, Maciej; Barqawi, Hiba Jawdat; Barra, Fabio; Barrow, Amadou; Basu, Sanjay; Belgaumi, Uzma Iqbal; Bhagavathula, Akshaya Srikanth; Bhardwaj, Nikha; Bhardwaj, Pankaj; Bhattacharjee, Natalia V.; Bhattacharyya, Krittika; Bijani, Ali; Bikbov, Boris; Boloor, Archith; Briko, Nikolay Ivanovich; Buonsenso, Danilo; Nagaraja, Sharath Burugina; Butt, Zahid A.; Carter, Austin; Carvalho, Felix; Charan, Jaykaran; Chatterjee, Souranshu; Chattu, Soosanna Kumary; Chattu, Vijay Kumar; Christopher, Devasahayam J.; Chu, Dinh-Toi; Claassens, Mareli M.; Dadras, Omid; Dagnew, Amare Belachew; Dai, Xiaochen; Dandona, Lalit; Dandona, Rakhi; Daneshpajouhnejad, Parnaz; Darwesh, Aso Mohammad; Dhamnetiya, Deepak; Dianatinasab, Mostafa; Diaz, Daniel; Doan, Linh Phuong; Eftekharzadeh, Sahar; Elhadi, Muhammed; Emami, Amir; Enany, Shymaa; Faraon, Emerito Jose A.; Farzadfar, Farshad; Fernandes, Eduarda; Desideri, Lorenzo Ferro; Filip, Irina; Fischer, Florian; Foroutan, Masoud; Frank, Tahvi D.; Garcia-Basteiro, Alberto L.; Garcia-Calavaro, Christian; Garg, Tushar; Geberemariyam, Biniyam Sahiledengle; Ghadiri, Keyghobad; Ghashghaee, Ahmad; Golechha, Mahaveer; Goodridge, Amador; Gupta, Bhawna; Gupta, Sapna; Gupta, Veer Bala; Gupta, Vivek Kumar; Haider, Mohammad Rifat; Hamidi, Samer; Hanif, Asif; Haque, Shaful; Harapan, Harapan; Hargono, Arief; Hasaballah, Ahmed I.; Hashi, Abdiwahab; Hassan, Shoaib; Hassankhani, Hadi; Hayat, Khezar; Hezam, Kamal; Holla, Ramesh; Hosseinzadeh, Mehdi; Hostiuc, Mihaela; Househ, Mowafa; Hussain, Rabia; Ibitoye, Segun Emmanuel; Ilic, Irena M.; Ilic, Milena D.; Irvani, Seyed Sina Naghibi; Ismail, Nahlah Elkudssiah; Itumalla, Ramaiah; Jaafari, Jalil; Jacobsen, Kathryn H.; Jain, Vardhmaan; Javanmardi, Fatemeh; Jayapal, Sathish Kumar; Jayaram, Shubha; Jha, Ravi Prakash; Jonas, Jost B.; Joseph, Nitin; Joukar, Farahnaz; Kabir, Zubair; Kamath, Ashwin; Kanchan, Tanuj; Kandel, Himal; Katoto, Patrick D.M.C.; Kayode, Gbenga A.; Kendrick, Parkes J.; Kerbo, Amene Abebe; Khajuria, Himanshu; Khalilov, Rovshan; Khatab, Khaled; Khoja, Abdullah T.; Khubchandani, Jagdish; Kim, Min Seo; Kim, Yun Jin; Kisa, Adnan; Kisa, Sezer; Kosen, Soewarta; Koul, Parvaiz A.; Laxminarayana, Sindhura Lakshmi Koulmane; Koyanagi, Ai; Krishan, Kewal; Bicer, Burcu Kucuk; Kumar, Avinash; Kumar, G. Anil; Kumar, Narinder; Kumar, Nithin; Kwarteng, Alexander; Lak, Hassan Mehmood; Lal, Dharmesh Kumar; Landires, Iv�n; Lasrado, Savita; Lee, Shaun Wen Huey; Lee, Wei-Chen; Lin, Christine; Liu, Xuefeng; Lopukhov, Platon D.; Lozano, Rafael; Machado, Daiane Borges; Kunjathur, Shilpashree Madhava; Madi, Deepak; Mahajan, Preetam Bhalchandra; Majeed, Azeem; Malik, Ahmad Azam; Martins-Melo, Francisco Rogerl�ndio; Mehta, Saurabh; Memish, Ziad A.; Mendoza, Walter; Menezes, Ritesh G.; Merie, Hayimro Edemealem; Mersha, Amanual Getnet; Mesregah, Mohamed Kamal; Mestrovic, Tomislav; Mheidly, Nour Mheidly; Misra, Sanjeev; Mithra, Prasanna; Moghadaszadeh, Masoud; Mohammadi, Mokhtar; Mohammadian-Hafshejani, Abdollah; Mohammed, Shafu; Molokhia, Mariam; Moni, Mohammad Ali; Al Montasir, Ahmed; Moore, Catrin E.; Nagarajan, Ahamarshan Jayaraman; Nair, Sanjeev; Nair, Suma; Naqvi, Atta Abbas; Swamy, Sreenivas Narasimha; Nayak, Biswa Prakash; Nazari, Javad; Kandel, Sandhya Neupane; Nguyen, Trang Huyen; Nixon, Molly R.; Nnaji, Chukwudi A.; Ntsekhe, Mpiko; Nu�ez-Samudio, Virginia; Oancea, Bogdan; Odukoya, Oluwakemi Ololade; Olagunju, Andrew T.; Oren, Eyal; Mahesh, P.A.; Parthasarathi, Ramakrishnan; Kan, Fatemeh Pashazadeh; Pattanshetty, Sanjay M.; Paudel, Rajan; Paul, Pintu; Pawar, Shrikant; Pepito, Veincent Christian Filipino; Perico, Norberto; Pirestani, Majid; Polibin, Roman V.; Postma, Maarten J.; Pourshams, Akram; Prashant, Akila; Pribadi, Dimas Ria Angga; Radfar, Amir; Rafei, Alireza; Rahim, Fakher; Rahimi-Movaghar, Vafa; Rahman, Mahfuzar; Rahman, Mosiur; Rahmani, Amir Masoud; Ranasinghe, Priyanga; Rao, Chythra R.; Rawaf, David Laith; Rawaf, Salman; Reitsma, Marissa B.; Remuzzi, Giuseppe; Renzaho, Andre M. N.; Reta, Melese Abate; Rezaei, Nima; Rezahosseini, Omid; Rezai, Mohammad Sadegh; Rezapour, Aziz; Roshandel, Gholamreza; Roshchin, Denis O.; Sabour, Siamak; Saif-Ur-rahman, K.M.; Salam, Nasir; Kafl, Hossein Samadi; Samaei, Mehrnoosh; Samy, Abdallah M.; Saroshe, Satish; Sartorius, Benn; Sathian, Brijesh; Sawyer, Susan M.; Senthilkumaran, Subramanian; Seylani, Allen; Shafaat, Omid; Shaikh, Masood Ali; Sharaf, Kiomars; Shetty, Ranjitha S.; Shigematsu, Mika; Shin, Jae Il; Silva, Jo�o Pedro; Singh, Jitendra Kumar; Sinha, Smriti; Skryabin, Valentin Yurievich; Skryabina, Anna Aleksandrovna; Spurlock, Emma Elizabeth; Sreeramareddy, Chandrashekhar T.; Steiropoulos, Paschalis; Sufyan, Mu'awiyyah Babale; Tabuchi, Takahiro; Tadesse, Eyayou Girma; Tamir, Zemenu; Tarkang, Elvis Enowbeyang; Tekalegn, Yohannes; Tesfay, Fisaha Haile; Tessema, Belay; Thapar, Rekha; Tleyjeh, Imad I.; Tobe-Gai, Ruoyan; Tran, Bach Xuan; Tsegaye, Berhan; Tsegaye, Gebiyaw Wudie; Ullah, Anayat; Umeokonkwo, Chukwuma David; Tahbaz, Sahel Valadan; Vo, Bay; Vu, Giang Thu; Waheed, Yasir; Walters, Magdalene K.; Whisnant, Joanna L.; Woldekidan, Mesfn Agachew; Wubishet, Befkadu Legesse; Jabbari, Seyed Hossein Yahyazadeh; Yazie, Taklo Simeneh Yazie; Yeshaw, Yigizie; Yi, Siyan; Yigit, Vahit; Yonemoto, Naohiro; Yu, Chuanhua; Yunusa, Ismaeel; Zastrozhin, Mikhail Sergeevich; Zastrozhina, Anasthasia; Zhang, Zhi-Jiang; Zumla, Alimuddin; Mokdad, Ali H.; Salomon, Joshua A.; Reiner, Robert C.; Lim, Stephen S.; Naghavi, Mohsen; Vos, Theo; Hay, Simon I.; Murray, Christopher J. L.; Kyu, Hmwe Hmwe
Background: Tuberculosis is a major contributor to the global burden of disease, causing more than a million deaths annually. Given an emphasis on equity in access to diagnosis and treatment of tuberculosis in global health targets, evaluations of differences in tuberculosis burden by sex are crucial. We aimed to assess the levels and trends of the global burden of tuberculosis, with an emphasis on investigating differences in sex by HIV status for 204 countries and territories from 1990 to 2019. Methods: We used a Bayesian hierarchical Cause of Death Ensemble model (CODEm) platform to analyse 21 505 site-years of vital registration data, 705 site-years of verbal autopsy data, 825 site-years of sample-based vital registration data, and 680 site-years of mortality surveillance data to estimate mortality due to tuberculosis among HIV-negative individuals. We used a population attributable fraction approach to estimate mortality related to HIV and tuberculosis coinfection. A compartmental meta-regression tool (DisMod-MR 2.1) was then used to synthesise all available data sources, including prevalence surveys, annual case notifications, population-based tuberculin surveys, and tuberculosis cause-specific mortality, to produce estimates of incidence, prevalence, and mortality that were internally consistent. We further estimated the fraction of tuberculosis mortality that is attributable to independent effects of risk factors, including smoking, alcohol use, and diabetes, for HIV-negative individuals. For individuals with HIV and tuberculosis coinfection, we assessed mortality attributable to HIV risk factors including unsafe sex, intimate partner violence (only estimated among females), and injection drug use. We present 95% uncertainty intervals for all estimates. Findings: Globally, in 2019, among HIV-negative individuals, there were 1�18 million (95% uncertainty interval 1�08�1�29) deaths due to tuberculosis and 8�50 million (7�45�9�73) incident cases of tuberculosis. Among HIV-positive individuals, there were 217 000 (153 000�279 000) deaths due to tuberculosis and 1�15 million (1�01�1�32) incident cases in 2019. More deaths and incident cases occurred in males than in females among HIV-negative individuals globally in 2019, with 342 000 (234 000�425 000) more deaths and 1�01 million (0�82�1�23) more incident cases in males than in females. Among HIV-positive individuals, 6250 (1820�11 400) more deaths and 81 100 (63 300�100 000) more incident cases occurred among females than among males in 2019. Age-standardised mortality rates among HIV-negative males were more than two times greater in 105 countries and age-standardised incidence rates were more than 1�5 times greater in 74 countries than among HIV-negative females in 2019. The fraction of global tuberculosis deaths among HIV-negative individuals attributable to alcohol use, smoking, and diabetes was 4�27 (3�69�5�02), 6�17 (5�48�7�02), and 1�17 (1�07�1�28) times higher, respectively, among males than among females in 2019. Among individuals with HIV and tuberculosis coinfection, the fraction of mortality attributable to injection drug use was 2�23 (2�03�2�44) times greater among males than females, whereas the fraction due to unsafe sex was 1�06 (1�05�1�08) times greater among females than males. Interpretation: As countries refine national tuberculosis programmes and strategies to end the tuberculosis epidemic, the excess burden experienced by males is important. Interventions are needed to actively communicate, especially to men, the importance of early diagnosis and treatment. These interventions should occur in parallel with efforts to minimise excess HIV burden among women in the highest HIV burden countries that are contributing to excess HIV and tuberculosis coinfection burden for females. Placing a focus on tuberculosis burden among HIV-negative males and HIV and tuberculosis coinfection among females might help to diminish the overall burden of tuberculosis. This strategy will be crucial in reaching both equity and burden targets outlined by global health milestones. Funding: Bill & Melinda Gates Foundation. � 2022 The Author(s). Published by Elsevier Ltd. This is an Open Access article under the CC BY 4.0 license
Human anaerobic microbiome: a promising and innovative tool in cancer prevention and treatment by targeting pyruvate metabolism
(Springer Science and Business Media Deutschland GmbH, 2023-10-26T00:00:00) Om, Hari; Chand, Umesh; Kushawaha, Pramod Kumar
Introduction: Even in present-day times, cancer is one of the most fatal diseases. People are overwhelmed by pricey chemotherapy, immunotherapy, and other costly cancer therapies in poor and middle-income countries. Cancer cells grow under anaerobic and hypoxic conditions. Pyruvate is the final product of the anaerobic glycolysis pathway, and many cancer cells utilize pyruvate for their growth and development. The anaerobic microbiome produces many anti-cancer substances that can act as anti-tumor agents and are both feasible and of low cost. There are different mechanisms of action of the anaerobic microbiome, such as the production of short-chain fatty acids (SCFAs), and competition for the anaerobic environment includes the metabolic product pyruvate to form lactic acid for energy. Key findings: In this review, we have summarized the role of the metabolic approach of the anaerobic human microbiome in cancer prevention and treatment by interfering with cancer metabolite pyruvate. SCFAs possess decisive outcomes in condoning almost all the hallmarks of cancer and helping the spread of cancer to other body parts. Studies have demonstrated the impact and significance of using SCFA, which results from anaerobic bacteria, as an anti-cancer agent. Anaerobic bacteria-based cancer therapy has become a promising approach to treat cancer using obligate and facultative anaerobic bacteria because of their ability to penetrate and increase in an acidic hypoxic environment. Significance: This review attempts to provide the interconnection of cancer metabolism and anaerobic microbiome metabolism with a focus on pyruvate metabolism to understand and design unique anaerobic microbiota-based therapy for cancer patients. Graphical abstract: [Figure not available: see fulltext.]. � 2023, The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.
Human anaerobic microbiome: a promising and innovative tool in cancer prevention and treatment by targeting pyruvate metabolism
(Springer Science and Business Media Deutschland GmbH, 2023-10-26T00:00:00) Om, Hari; Chand, Umesh; Kushawaha, Pramod Kumar
Introduction: Even in present-day times, cancer is one of the most fatal diseases. People are overwhelmed by pricey chemotherapy, immunotherapy, and other costly cancer therapies in poor and middle-income countries. Cancer cells grow under anaerobic and hypoxic conditions. Pyruvate is the final product of the anaerobic glycolysis pathway, and many cancer cells utilize pyruvate for their growth and development. The anaerobic microbiome produces many anti-cancer substances that can act as anti-tumor agents and are both feasible and of low cost. There are different mechanisms of action of the anaerobic microbiome, such as the production of short-chain fatty acids (SCFAs), and competition for the anaerobic environment includes the metabolic product pyruvate to form lactic acid for energy. Key findings: In this review, we have summarized the role of the metabolic approach of the anaerobic human microbiome in cancer prevention and treatment by interfering with cancer metabolite pyruvate. SCFAs possess decisive outcomes in condoning almost all the hallmarks of cancer and helping the spread of cancer to other body parts. Studies have demonstrated the impact and significance of using SCFA, which results from anaerobic bacteria, as an anti-cancer agent. Anaerobic bacteria-based cancer therapy has become a promising approach to treat cancer using obligate and facultative anaerobic bacteria because of their ability to penetrate and increase in an acidic hypoxic environment. Significance: This review attempts to provide the interconnection of cancer metabolism and anaerobic microbiome metabolism with a focus on pyruvate metabolism to understand and design unique anaerobic microbiota-based therapy for cancer patients. Graphical abstract: [Figure not available: see fulltext.]. � 2023, The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.
Interferon inducible guanylate binding protein 1 restricts the growth of Leishmania donovani by modulating the level of cytokines/chemokines and MAP kinases
(Academic Press, 2022-05-09T00:00:00) Kumar, Ravindra; Kushawaha, Pramod Kumar
Visceral Leishmaniasis (VL) is a zoonotic chronic endemic infectious disease caused by Leishmania donovani infection and a well-studied model for intracellular parasitism. Guanylate binding proteins (GBPs) are induced by interferons (IFNs), and play a crucial role in cell autonomous immunity and the regulation of inflammation. Guanylate-binding protein 1 (GBP1) has been shown vital for the host immune response against various pathogens. However, the role of GBP1 during VL is undefined. In the present study, we have investigated the role of GBP1 in Leishmania donovani infection using in vitro model. For that, knock down of the Gbp1 gene was carried out in both PMA differentiated human monocyte cell line THP-1 and mouse macrophages RAW264.7 cell line using siRNA based RNA interference. Infection of these cell lines revealed a high parasite load in knock down cells at 24 and 48h post infection as compared to control cells. A significant increase was observed in the level of different cytokines (IL-4, IL-10, IL-12b, IFN-?, TNF-?) and chemokines (CXCL9, CXCL 10, and CXCL 11) in GBP1 knock down cell lines after post-infection. In GBP1 knock down cells the expression level of IFN effector molecules (iNOS and PKR) was found to be elevated in THP1 cells and remained almost unchanged in RAW264.7 cells after Leishmania donovani infection as compared to the control cells. Moreover, interestingly, the level of MAPK activated ERK1/2, and p38 MAPK were considerably induced by the parasite in knock down cells as compared to control after 24 h post-infection. This study, first time reported the involvement of GBP1 in Leishmania donovani infection by modulating the level of important cytokines, chemokines, IFN effector molecules, and MAP kinases. � 2022 Elsevier Ltd
Interferon inducible guanylate binding protein 1 restricts the growth of Leishmania donovani by modulating the level of cytokines/chemokines and MAP kinases
(Academic Press, 2022-05-09T00:00:00) Kumar, Ravindra; Kushawaha, Pramod Kumar
Visceral Leishmaniasis (VL) is a zoonotic chronic endemic infectious disease caused by Leishmania donovani infection and a well-studied model for intracellular parasitism. Guanylate binding proteins (GBPs) are induced by interferons (IFNs), and play a crucial role in cell autonomous immunity and the regulation of inflammation. Guanylate-binding protein 1 (GBP1) has been shown vital for the host immune response against various pathogens. However, the role of GBP1 during VL is undefined. In the present study, we have investigated the role of GBP1 in Leishmania donovani infection using in vitro model. For that, knock down of the Gbp1 gene was carried out in both PMA differentiated human monocyte cell line THP-1 and mouse macrophages RAW264.7 cell line using siRNA based RNA interference. Infection of these cell lines revealed a high parasite load in knock down cells at 24 and 48h post infection as compared to control cells. A significant increase was observed in the level of different cytokines (IL-4, IL-10, IL-12b, IFN-?, TNF-?) and chemokines (CXCL9, CXCL 10, and CXCL 11) in GBP1 knock down cell lines after post-infection. In GBP1 knock down cells the expression level of IFN effector molecules (iNOS and PKR) was found to be elevated in THP1 cells and remained almost unchanged in RAW264.7 cells after Leishmania donovani infection as compared to the control cells. Moreover, interestingly, the level of MAPK activated ERK1/2, and p38 MAPK were considerably induced by the parasite in knock down cells as compared to control after 24 h post-infection. This study, first time reported the involvement of GBP1 in Leishmania donovani infection by modulating the level of important cytokines, chemokines, IFN effector molecules, and MAP kinases. � 2022 Elsevier Ltd