Abstract
Recent work from our laboratory has provided evidence that indicates selective bacterial translocation from the host gut microbiota to peripheral tissues (i.e. lung) plays a key role in the development of post-stroke infections. Despite this, it is currently unknown whether mucosal bacteria that live on and interact closely with the host intestinal epithelium contribute in regulating bacterial translocation after stroke. Here, we found that the microbial communities within the mucosa of gastrointestinal tract (GIT) were significantly different between sham-operated and post-stroke mice at 24 h following surgery. The differences in microbiota composition were substantial in all sections of the GIT and were significant, even at the phylum level. The main characteristics of the stroke-induced shift in mucosal microbiota composition were an increased abundance of Akkermansia muciniphila and an excessive abundance of clostridial species. Furthermore, we analysed the predicted functional potential of the altered mucosal microbiota induced by stroke using PICRUSt and revealed significant increases in functions associated with infectious diseases, membrane transport and xenobiotic degradation. Our findings revealed stroke induces far-reaching and robust changes to the intestinal mucosal microbiota. A better understanding of the precise molecular events leading up to stroke-induced mucosal microbiota changes may represent novel therapy targets to improve patient outcomes.
Highlights
Recent work from our laboratory has provided evidence that indicates selective bacterial translocation from the host gut microbiota to peripheral tissues plays a key role in the development of post-stroke infections
We analysed and compared the microbial communities associated with mucosa across five gastrointestinal tract (GIT) sections: duodenum, jejunum, ileum, cecum, and colon, between the sham-operated and post-stroke mice at 24 h
The significant increase in presence of clostridia in proximity to gut barrier is in agreement with clostridial species we previously reported as migrated bacteria to post-stroke lung[10]
Summary
Recent work from our laboratory has provided evidence that indicates selective bacterial translocation from the host gut microbiota to peripheral tissues (i.e. lung) plays a key role in the development of post-stroke infections. It is currently unknown whether mucosal bacteria that live on and interact closely with the host intestinal epithelium contribute in regulating bacterial translocation after stroke. Recent work from our laboratory has provided evidence that indicates selective bacterial translocation from the host gut microbiota to peripheral tissues (i.e. lung) plays a key role in the development of these post-stroke infections[10], implicating gut epithelial mucosa and intestinal microbiota as the main players in post-stroke mortality. Being closest to the host epithelium, we propose that the mucosal microbiota is the prime location to respond to stroke injury and potentially has the opportunity to either invade the host or launch epithelial healing responses to re-establish gut barrier integrity after stroke
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