Regular exercise reprograms bone marrow macrophages, inducing lasting mitochondrial changes that accumulate, driving a tempered inflammatory response.
Although inflammation is a critical component of the body’s immune response, excess inflammation drives many chronic diseases, such as autoimmune disorders, cardiovascular diseases, diabetes, and cancer. A new study in mice shows that regular exercise reprograms macrophages, altering how they sense and respond to pathogens and reducing inflammation.
Macrophages are immune cells that participate in pathogen elimination via phagocytosis. Distinguished by their polarization, “M1” macrophages exhibit a proinflammatory phenotype, while “M2” macrophages exhibit an anti-inflammatory phenotype. A high M1 to M2 ratio indicates inflammation and a chronic disease state.
Researchers collected macrophages from the bone marrow of two groups of mice – one that had exercised regularly for eight weeks and one that had been sedentary. Then they exposed the macrophages to lipopolysaccharide (a bacterial toxin that induces an acute inflammatory reaction) and assessed the cells' responses.
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They found that macrophages from the exercised mice exhibited decreased activation of NF-κB, the primary transcription factor of M1 macrophages. The macrophages also demonstrated reduced expression of inflammation-related genes, increased expression of M2 macrophage-associated genes, and improved mitochondrial function.
These findings suggest that regular exercise modulates macrophages' responses to inflammation by enhancing their respiratory capacity and altering gene expression, with potential implications for preventing or treating inflammatory diseases. Read more about the benefits of exercise in our overview article.