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Background   Mycobacterium smegmatis , a rapidly growing non-tuberculosis mycobacterium, is a good model for studying the pathogenesis of tuberculosis because of its genetic similarity to  Mycobacterium tuberculosis  (Mtb). Macrophages remove mycobacteria during an infection. Macrophage apoptosis is a host defense mechanism against intracellular bacteria. We have reported that endoplasmic reticulum (ER) stress is an important host defense mechanism against Mtb infection.    Results  In this study, we found that  M. smegmatis  induced strong ER stress.  M. smegmatis -induced reactive oxygen species (ROS) play a critical role in the induction of ER stress-mediated apoptosis. Pretreatment with an ROS scavenger suppressed  M. smegmatis -induced ER stress. Elimination of ROS decreased the ER stress response and significantly increased the intracellular survival of  M. smegmatis . Interestingly, inhibition of phagocytosis significantly decreased ROS synthesis, ER stress response induction, and cytokine production.    Conclusions  Phagocytosis of  M. smegmatis  induces ROS production, leading to production of proinflammatory cytokines. Phagocytosis-induced ROS is associated with the  M. smegmatis -mediated ER stress response in macrophages. Therefore, phagocytosis plays a critical role in the induction of ER stress-mediated apoptosis during mycobacterial infection.

Phagocytosis influences the intracellular survival of Mycobacterium smegmatis via the endoplasmic reticulum stress response