The intestinal barrier function is crucial in maintaining the host's homeostasis, as it acts as the first protective barrier between the lumenal content and circulation. Disruptions to this protective barrier have been linked to various pathological conditions. Excessive permeability can lead to tissue damage, systemic inflammation, and even organ failure. Studies have shown that the gut microbiota and its metabolites have an essential role in the regulation of the intestinal barrier function. Negative alterations to the gut microbiota, known as dysbiosis, have been shown to be a factor involved for the increased barrier permeability. Thus, restoration of the gut microbiota can provide a novel approach for the prevention of adverse effects caused by the loss of this protective barrier. The main goal of this study was to evaluate the efficacy of a prebiotic and probiotic in maintaining the intestinal barrier integrity during heat stress.

Animals were pre‐treated by oral gavage with Bacillus subtilis probiotic strain, a yeast fermentate product having prebiotic properties, or phosphate buffered saline (PBS) prior to exposure to heat stress. Control rats received identical treatments, but without the exposure to stressor. The results demonstrated that heat stress lead to significant changes to the intestinal barrier in the stressed animals pre‐treated with PBS, causing significant decreases in villi height and total mucosal thickness, and reduced expression of tight junction proteins. The level of lipopolysaccharides in serum also significantly increased in those animals. All registered adverse effects were prevented in stressed animals pre‐treated with the probiotic and prebiotic. Analysis of the gut microbiota revealed significant disruption of microbial composition only in the stressed rats pre‐treated with PBS. These results demonstrate the high efficacy of the prebiotic and probiotic in preventing the loss of the intestinal barrier function. We can speculate that the beneficial modulation of the gut microbiota could be a valuable approach for prevention of stress‐related adverse effects.

Support or Funding Information

This work was supported by Auburn University funds.

This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.