School Of Basic And Applied Sciences

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Subject: search.filters.subject.Cytokines

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Now showing 1 - 5 of 5
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    Implicative role of cytokines in neuroinflammation mediated AD and associated signaling pathways: Current progress in molecular signaling and therapeutics
    (Elsevier Ireland Ltd, 2023-10-30T00:00:00) Kumari, Sneha; Dhapola, Rishika; Sharma, Prajjwal; Singh, Sunil K.; Reddy, Dibbanti HariKrishna
    Alzheimer's Disease (AD) is one of the most devastating age-related disorder causing significant social and economic burden worldwide. It affects the cognitive and social behavior of individuals and characterized by accumulation of A?, phosphorylated tau and cytokines formation. The synthesis and release of cytokines are regulated by specific groups of immune and non-immune cells in response to microglia or astrocyte activation through multiple pathways. Physiologically, microglia assert an anti-inflammatory, quiescent state with minimal cytokine expression and little phagocytic activity in motion to carry out their housekeeping role to eliminate pathogens, aggregated A? and tau protein. However, they develop a phagocytic nature and overexpress cytokine gene modules in response to certain stimuli in AD. Microglia and astrocytes upon chronic activation release an enormous amount of inflammatory cytokines due to interaction with formed A? and neurofibrillary tangle. Gut microbiota dysbiosis also stimulates the release of inflammatory cytokines contributing to AD pathogenesis. In addition, the dysregulation of few signaling pathways significantly influences the development of disease, and the pace of advancement also rises with age. This review sheds light on multiple pathways results into neuroinflammation triggered by activated cytokines worsening AD pathology and making it an appropriate target for AD treatment. This review also included drugs targeting different neuroinflammation pathways under clinical and preclinical studies that are found to be effective in attenuating the disease pathology. � 2023 Elsevier B.V.
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    Cloning, expression and in vitro validation of chimeric multi epitope vaccine candidate against visceral leishmaniasis infection
    (Elsevier Inc., 2023-04-11T00:00:00) Ojha, Rupal; Chand, Kailash; Vellingiri, Balachandar; Prajapati, Vijay Kumar
    Visceral Leishmaniasis or Kala-Azar is one of the most severe and deadly neglected tropical disease caused by the Leishmania parasite. A few number of vaccines are going through different phases in clinical trial but failing of these vaccines in successive phase trial or less efficacy, urge to develop highly immunogenic and cost-effective treatment to get rid of deadly VL. This study focuses on the development of more potent vaccine candidate against VL. The recombinant vaccine candidate LeiSp was expressed in Pichia pastoris, followed by purification and characterization. The purified protein was also tested for any post-translation modification, which favors being a potent immunogenic candidate. Further, the expression modulation of different pro-inflammatory and anti-inflammatory cytokines was evaluated in THP1 cell lines. A significant upregulation in the expression of pro-inflammatory cytokines while no significant changes were observed in the expression of anti-inflammatory cytokines. The impact of recombinant vaccine protein candidates in infected conditions were determined. Here, upon treatment with chimeric vaccine protein candidate, we observed a considerable recovery in the expression level of pro-inflammatory cytokines, which were downregulated upon infection alone. In addition to this, we found a significant decrease in the expression of anti-inflammatory cytokines, which were upregulated during infection alone. We further validated our findings in infected hPBMCs and observed similar expression modulation of pro-inflammatory and anti-inflammatory cytokines with and without treatment. Thus, the present study indicates that the chimeric LeiSp protein which was designed using bioinformatics approaches shows a potential inductive efficacy for pro-inflammatory cytokines in Leishmania-infected cells. � 2023 Elsevier Inc.
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    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
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    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
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    Understanding Immune-etiology of Psoriasis: An autoimmune disease
    (Central University of Punjab, 2018) Kumari, Anjna; Jain, Manju
    Psoriasis is a chronic inflammatory autoimmune disease. Disease etiology is understood in terms of altered crosstalk between skin keratinocytes and immune cell infiltrates, specifically T cells leading to the development of characteristic psoriatic skin lesions. T cell alterations in skin lesions as well as in the peripheral blood of psoriatic patients have been shown to be associated with the disease condition. With a major research focus on keratinocyte abnormalities, more studies are required to understand the immune-etiology of disease. There are fewer reports with inconsistence findings on T cell changes in psoriatic patients. Towards this end, we performed a study using blood samples from psoriasis patients and healthy controls to access alterations in peripheral blood mononuclear cell and T cell count along with phenotyping of blood cells in terms of CD4+ Th and CD8+ Tc cells and expression pattern of T cell-associated cytokines in plasma samples. Furthermore, TREC analysis was done to understand possible origin of T cell alterations associated with psoriasis.