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Vancomycin treatment and butyrate supplementation modulate gut microbe composition and severity of neointimal hyperplasia after arterial injury
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Vancomycin treatment and butyrate supplementation modulate gut microbe composition and severity of neointimal hyperplasia after arterial injury
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Journal Article
Vancomycin treatment and butyrate supplementation modulate gut microbe composition and severity of neointimal hyperplasia after arterial injury
2015
Overview
Gut microbial metabolites are increasingly recognized as determinants of health and disease. However, whether host–microbe crosstalk influences peripheral arteries is not understood. Neointimal hyperplasia, a proliferative and inflammatory response to arterial injury, frequently limits the long‐term benefits of cardiovascular interventions such as angioplasty, stenting, and bypass surgery. Our goal is to assess the effect of butyrate, one of the principal short chain fatty acids produced by microbial fermentation of dietary fiber, on neointimal hyperplasia development after angioplasty. Treatment of male Lewis Inbred rats with oral vancomycin for 4 weeks changed the composition of gut microbes as assessed by 16S rRNA‐based taxonomic profiling and decreased the concentration of circulating butyrate by 69%. In addition, rats treated with oral vancomycin had exacerbated neointimal hyperplasia development after carotid angioplasty. Oral supplementation of butyrate reversed these changes. Butyrate also inhibited vascular smooth muscle cell proliferation, migration, and cell cycle progression in a dose‐dependent manner in vitro. Our results suggest for the first time that gut microbial composition is associated with the severity of arterial remodeling after injury, potentially through an inhibitory effect of butyrate on VSMC. This report demonstrates that antibiotic modulation of gut microbial composition alters production of a microbe‐derived metabolite, sodium butyrate, which then regulates the arterial remodeling response after balloon angioplasty in rats. One potential mechanism is inhibition of vascular smooth muscle cell proliferation, migration, and cell cycle progression by butyrate.
Publisher
John Wiley & Sons, Inc,John Wiley and Sons Inc
