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Mycobacterium tuberculosis (Mtb) is known to be responsible for tuberculosis (TB), but the pathogenesis of this disease and the host defense mechanisms involved are, for the most part, poorly understood. In this study, we divided 30 male C57BL/6 mice into control and infection groups, and following injection with physiological saline or Mtb, respectively, euthanized five mice from each group on days 1, 3, and 7. TNF-α and IL-10 levels were measured by enzyme-linked immunosorbent assay and flow cytometry, with the latter also being performed to assess apoptosis rates. Protein expression of STAT3 and its phosphorylated form (p-STAT3) was analyzed by western blotting. After Mtb infection, TNF-α and IL-10 levels, alveolar macrophage apoptosis, and STAT3 and p-STAT3 expression increased significantly on days 1, 3, and 7 (P &lt; 0.05), with maximum values on day 3. Furthermore, the Pearson correlation test showed that production of the cytokines TNF-α and IL-10 correlated strongly with expression of STAT3 and p-STAT3 proteins (P &lt; 0.05). Taken together, our results suggest that the STAT3 signaling pathway might play a key role in the regulation of cell proliferation and alveolar macrophage apoptosis in response to Mtb. This provides a theoretical mechanism behind TB pathogenesis and host defense against Mtb, and contributes towards development of an effective treatment.

Role of IL-10 and TNF-α during Mycobacterium tuberculosis infection in murine alveolar macrophages