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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.

The Key Role of c-Fos for Immune Regulation and Bacterial Dissemination in Brucella Infected Macrophage