Title |
The Key Role of c-Fos for Immune Regulation and Bacterial Dissemination in Brucella Infected Macrophage
|
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Published in |
Frontiers in Cellular and Infection Microbiology, August 2018
|
DOI | 10.3389/fcimb.2018.00287 |
Pubmed ID | |
Authors |
Huynh T. Hop, Lauren T. Arayan, Tran X. N. Huy, Alisha W. B. Reyes, Son H. Vu, WonGi Min, Hu J. Lee, Man H. Rhee, Hong H. Chang, Suk Kim |
Abstract |
The cellular oncogene c-Fos (c-Fos) is a component of activator protein 1 (AP1), a master transcriptional regulator of cells. The suppression of c-Fos signaling by siRNA treatment resulted in significant induction of TLR4, which subsequently activates p38 and ERK1/2 mitogen-activated protein kinases (MAPKs) and enhances F-actin polymerization, leading to an increase in B. abortus phagocytosis. During B. abortus infection, c-Fos signaling is induced, which activates the downstream innate-immunity signaling cascade for bacterial clearance. The inhibition of c-Fos signaling led to increased production of interleukin 10 (IL-10), which partially suppressed lysosome-mediated killing, resulting in increased survival of B. abortus inside macrophages. We present evidence of the regulatory role played by the c-Fos pathway in proliferation during B. abortus infection; however, this was independent of the anti-Brucella effect of this pathway. Another finding is the essential contribution of c-Fos/TRAIL to infected-cell necrosis, which is a key event in bacterial dissemination. These data provide the mechanism via which c-Fos participates in host defense mechanisms against Brucella infection and in bacterial dissemination by macrophages. |
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