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European journal of molecular biology and biochemistry

Volume 11, Issue 1, 2024
Mcmed International
European journal of molecular biology and biochemistry
Issn
2348 - 2192 (Print), 2348 - 2206 (Online)
Frequency
bi-annual
Email
editorejmbb@mcmed.us
Journal Home page
http://mcmed.us/journal/ejmbb
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Abstract
Title
MECHANISMS OF BRUCELLA ABORTUS-INDUCED OSTEOCLASTOGENESIS: IMPLICATIONS FOR BONE LOSS IN INFECTION
Author
Sudha Parimala S
Email
Sudha Parimala S@gmail.com
keyword
Brucella abortus, Osteoclastogenesis, T lymphocytes, Bone loss, Cytokines
Abstract
The underlying mechanisms by which Brucella species induce bone loss remain unclear, posing challenges for effective infection control. This study investigates Brucella abortusinduced T lymphocyte (LT) responses and their role in osteoclastogenesis, a key process linked to bone density reduction. Brucella-induced inflammation activates LTs, promoting osteoclastogenesis in both in vitro and in vivo models. Culture supernatant from B. abortus-infected macrophages stimulates osteoclastogenesis in bone marrow-derived monocytes. CD4+ T cells are identified as mediators of osteoclastogenesis, and critical cytokines, RANKL and IL-17, secreted by B. abortus-activated T cells, play essential roles in this process. The study further reveals the involvement of IL-6 in promoting LT-derived pro-osteoclastogenic IL-17 during Brucella infection. Additionally, IL-17 indirectly induces osteoclastogenesis through the induction of tumor necrosis factor-?. These findings provide valuable insights into the complex interplay between Brucella infection, T cell activation, and bone loss, emphasizing the significance of understanding these mechanisms for developing targeted therapeutic strategies.
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