Regular exercise improves inflammatory responses by resident or recruited macrophages against bacterial pathogens
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Regular, moderate-intensity exercise is beneficial to host defenses against infections. Such exercise regimes improve the inflammatory and bactericidal potencies of macrophages, cells that are crucial in activating both innate and adaptive immune responses. The M1 type (classical) macrophage activation after recognition of the pathogen-associated molecular patterns, such as lipopolysaccharide (LPS), induces pro-inflammatory responses in infected foci; these responses are necessary to effectively clear the pathogens. We reported previously that a 3-week-long treadmill exercise program enhanced LPS-induced interleukin (IL)12 mRNA expression and IL-12 secretion by downregulating 2-adrenergic receptor expression in the murine peritoneal resident macrophages, suggesting that regular exercise promotes the Toll-like receptor signaling and expression of its target genes in resident macrophages. We also reported that an 8-week-long, voluntary wheel-running exercise program potentiated LPS-induced IL-1 and IL-18 secretion without affecting the intracellular pro-IL-1 or pro-IL-18 mRNA or protein levels in the thioglycollate-elicited peritoneal murine macrophages. This program increased the intracellular caspase-1 protein levels. These results suggest that regular exercise promotes pro-IL-1 and pro-IL-18 maturation by increasing the levels of the inflammasome-activated caspase-1 in the recruited macrophages. Here, we review our collective studies and compare the mechanistic differences by which regular exercise improves pro-inflammatory responses to bacterial pathogens by resident or recruited macrophages.
