Microbial co-infection alters phagocytic potential, cellular responses and intramacrophage bacterial replication
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Abstract
Humans encounter multiple microorganisms every day. These microorganisms enter the host and interact with sentinel phagocytic cells such as macrophages. The macrophages engulf the microbes which get processed through the endocytic pathway. Many pathogens target macrophages and subvert the endocytic pathway and replicate inside these cells. It is more than likely that two different pathogens will be phagocytosed by the same macrophage. During such an encounter the host response generated by one pathogen will have its implications on the other pathogen present. In the current study, prior infection with Mycobacterium bovis BCG activates the macrophage to produce pro-inflammatory cytokines and nitric oxide, which helps it to control a subsequent Francisella tularensis LVS infection. The same effect is not seen in alternatively activated macrophages which do not produce nitric oxide. Overall, this study establishes a model to highlight different activation states of a macrophage and how different pathogens have the potential to modulate the host response.