An insight into intestinal mucosal microbiota disruption after stroke

Dragana Stanley, Robert J. Moore, Connie H. Y. Wong

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.