Recovery from antibiotic destruction of microbiota reveals immune cell mediator of neurogenesis

Lack of antibiotic management and overuse has generated far reaching effects just in the context of antibiotic resistance. Beyond the threat of generating a superbug, emerging evidence now suggests that we weigh the threat of antibiotics themselves. Researchers from the University of Magdeburg, Germany have pointed to a delicate balance between immune cells, gut microbiota, and neurogenesis, disrupted by antibiotic administration. Upon noting a decrease in hippocampal neurogenesis in adult mice post-antibiotic treatment, researchers sought to reconstitute plasticity. Fecal transplant replacement of gut flora failed to restore function without inclusion of probiotics or exercise. Adding further complexity, the response is connected to innate immune cells, as the Ly6Chi monocyte population was found to be dramatically decreased after antibiotic treatment. Accordingly, gut flora reconstitution accompanied with probiotics or exercise increased the same pool of cells. Furthermore, adoptive Ly6Chi monocyte transfer to knockout or antibody treated mice rescued neurogenesis in vivo. Cell transfer also promoted sphere formation by neural progenitor cells in vitro, further demonstrating the integral role of these innate immune cells in regards to the mechanism of communication along this gut-brain axis.


Möhle, et. al. Ly6Chi Monocytes Provide a Link between Antibiotic-Induced Changes in Gut Microbiota and Adult Hippocampal Neurogenesis CELL REPORTS


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