Repository logo
Communities & Collections
All of DSpace
  • English
  • العربية
  • বাংলা
  • Català
  • Čeština
  • Deutsch
  • Ελληνικά
  • Español
  • Suomi
  • Français
  • Gàidhlig
  • हिंदी
  • Magyar
  • Italiano
  • Қазақ
  • Latviešu
  • Nederlands
  • Polski
  • Português
  • Português do Brasil
  • Srpski (lat)
  • Српски
  • Svenska
  • Türkçe
  • Yкраї́нська
  • Tiếng Việt
Log In
New user? Click here to register.Have you forgotten your password?
  1. Home
  2. Browse by Author

Browsing by Author "Yadav V.K."

Filter results by typing the first few letters
Now showing 1 - 1 of 1
  • Results Per Page
  • Sort Options
  • No Thumbnail Available
    Item
    Crosstalk between platelet and bacteria: A therapeutic prospect
    (Bentham Science Publishers, 2019) Yadav V.K.; Singh P.K.; Agarwal V.; Singh S.K.
    Platelets are typically recognized for their roles in the maintenance of hemostasis and vascular wall repair to reduce blood loss. Beyond hemostasis, platelets also play a critical role in pathophysiological conditions like atherosclerosis, stroke, thrombosis, and infections. During infection, platelets interact directly and indirectly with bacteria through a wide range of cellular and molecular mechanisms. Platelet surface receptors such as GPIb?, Fc?RIIA, GPIIbIIIa, and TLRs, etc. facilitate direct interaction with bacterial cells. Besides, the indirect interaction between platelet and bacteria involves host plasma proteins such as von Willebrand Factor (vWF), fibronectin, IgG, and fibrinogen. Bacterial cells induce platelet activation, aggregation, and thrombus formation in the microvasculature. The activated platelets induce the Neutrophil Extracellular Traps (NETs) formation, which further contribute to thrombosis. Thus, platelets are extensively anticipated as vital immune modulator cells during infection, which may further lead to cardiovascular complications. In this review, we cover the interaction mechanisms between platelets and bacteria that may lead to the development of thrombotic disorders. Platelet receptors and other host molecules involved in such interactions can be used to develop new therapeutic strategies to combat against infection-induced cardiovascular complications. In addition, we highlight other receptor and enzyme targets that may further reduce infection-induced platelet activation and various pathological conditions.

DSpace software copyright © 2002-2025 LYRASIS

  • Privacy policy
  • End User Agreement
  • Send Feedback
Repository logo COAR Notify