Dynamic changes to the intestinal environment occur throughout recovery from experimental ischemic stroke.

Abstract

Stroke survivors can experience a plethora of complications throughout their recovery that impair quality of life and impact neurological outcomes. Intestinal dysfunction is reported to occur rapidly following stroke in both humans and animal models and alterations such as reduced barrier integrity, lymphocyte loss and an altered microbiota have been suggested to contribute to increased brain injury. Despite the persistence of gastrointestinal symptoms in many stroke survivors, how the intestinal environment changes over the course of stroke recovery remains poorly understood. Here, we use an experimental model of ischaemic stroke to determine if gastrointestinal dysfunction persists into chronic recovery. We have shown that experimental stroke leads to structural alterations to the colon, a thinned mucus barrier, impaired transit times and an altered bacterial community composition. While barrier function and transit times recover within 2 weeks, structural and bacterial community alterations remain up to 3 months after stroke and are accompanied by altered luminal antibody profiles. Together, this suggests that the gastrointestinal system is dynamically altered over the course of experimental stroke recovery and highlight intestinal dysfunction as a target to improve patient outcomes beyond the acute recovery window.