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Mycobacterium tuberculosis  is a successful intracellular pathogen. Numerous host innate immune responses signaling pathways are induced upon mycobacterium invasion, however their impact on  M. tuberculosis  replication is not fully understood. Here we reinvestigate the role of STAT3 specifically inside human macrophages shortly after  M. tuberculosis  uptake. We first show that STAT3 activation is mediated by IL-10 and occurs in  M. tuberculosis  infected cells as well as in bystander non-colonized cells. STAT3 activation results in the inhibition of IL-6, TNF-α, IFN-γ and MIP-1β. We further demonstrate that STAT3 represses iNOS expression and NO synthesis. Accordingly, the inhibition of STAT3 is detrimental for  M. tuberculosis  intracellular replication. Our study thus points out STAT3 as a key host factor for  M. tuberculosis  intracellular establishment in the early stages of macrophage infection.

STAT3 Represses Nitric Oxide Synthesis in Human Macrophages upon Mycobacterium tuberculosis Infection