TY - JOUR ID - 125792 TI - Gene Silencing of Toll-like Receptor 2 Gene Expression as a Tactic to Control Mycobacterium Tuberculosis and Granuloma Formation JO - Archives of Razi Institute JA - ARI LA - en SN - 0365-3439 AU - Nama, M. A AD - Microbiology, Basic Medical Science Department, Nursing College, Iraq Y1 - 2022 PY - 2022 VL - 77 IS - 2 SP - 827 EP - 834 KW - BCG KW - THP-1 cells model KW - PPARγ KW - TLR2 siRNA knockdown DO - 10.22092/ari.2022.357152.1984 N2 - Mycobacterium tuberculosis (MT) is the causative agent of tuberculosis (TB) in humans. Tuberculosis is one of the top 10 causes of mortality worldwide, resulting in 1.8 million deaths and 10.4 million new cases in 2016. Understanding the fundamental features of MT biology is critical to the eradication of MT in the future. Due to the increasing frequency of antimicrobial treatment resistance and problems in vaccine development, the pathogenesis of TB for its survival and growth is highly dependent on host lipids and stimulated-lipid droplets formation. Toll-like receptor 2 (TLR2) forms heterophilic dimers with TLR1 and TLR6, therefore, recognizing many MT components. Both of these receptors identify the invading antigen and activate downstream protein kinases. Some studies demonstrated that the cyclooxygenase-2 (COX-2) promoter-driven gene expression includes connecting sites for transcription factors, such as nuclear factor-kappa B, CREB, NFAT, and c/EBPβ. The current study aimed to investigate the role of the TLR2 receptor in positively regulating prostaglandin E2 production in M. bovis (BCG) infected macrophages in vivo using a human monocytic cell line THP-1. Our results revealed that MT infection triggers a time-dependent increase in COX-2 expression via pathways involving TLR2 receptor activation and enhances COX-2 expression, leading to an increase in lipid droplet formation and suppression of macrophage activation. UR - https://archrazi.areeo.ac.ir/article_125792.html L1 - https://archrazi.areeo.ac.ir/article_125792_15f5818391cf13f3e88de6fa188b8dff.pdf ER -