Frontiers in Immunology · 13 authors, 3 centres
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In a mouse model, vancomycin given during the preweaning period induced CCR2-dependent recruitment of pro-inflammatory bone-marrow-derived macrophages into the colon, which increased phagocytosis of myenteric neurons and reduced enteric neuron density. These effects were specific to the neonatal period and were not observed in postweaning mice.
The authors demonstrate that vancomycin treatment in preweaning mice triggers CCR2-dependent recruitment of bone-marrow-derived monocytes/macrophages into the colon, which adopt a pro-inflammatory phenotype and increase phagocytosis of colonic myenteric neurons, resulting in reduced neuronal density. Vancomycin also decreased luminal serotonin levels in neonatal mice. The effects were restricted to the preweaning period; postweaning vancomycin treatment did not alter neuronal density or expand the macrophage population. CCR2-deficient mice were protected from the vancomycin-induced neuronal density reduction. The findings suggest a mechanism by which early-life antibiotic exposure disrupts enteric nervous system development through macrophage-mediated neuronal engulfment.
