Faecalibacterium prausnitzii and a Prebiotic Protect Intestinal Health in a Mouse Model of Antibiotic and Clostridium difficile Exposure

Abstract

Background Clostridium difficile (CD) infection (CDI) increases patient morbidity, mortality and healthcare costs. Antibiotic treatment induces gut dysbiosis and is both a major risk factor for CD colonization and treatment of CDI. Probiotics have been trialed to support commensal gut microbiota and reduce CDI. This study investigated commensal microbe Faecalibacterium prausnitzii (FP) and a prebiotic, both known to yield butyrate and be anti-inflammatory and immunomodulatory, on CD colonization and gut integrity in mice. Methods Mice were randomly grouped and supplemented daily with FP, prebiotic, FP + prebiotic, FP/prebiotic supernatant, or saline throughout the entire study. Following treatment with clindamycin for 3 days, mice were exposed to CD. Feces were collected at baseline, the day after antibiotic, and 1, 3, and 5 days after CD exposure and cultured for bacterial overgrowth and CD colonization. On days 1 and 5 after CD exposure, mice were randomly euthanized, and proximal colon was dissected for histological analysis and preparation of RNA for analysis of proinflammatory and anti-inflammatory cytokines. Results Although all mice exhibited bacterial overgrowth and CD colonization, bacterial burden resolved quicker in the FP + prebiotic group. This was associated with induction and resolution of innate immune responses, anion exchanger, and tight junction protein preservation in proximal colon. CD toxin virulence potential was questionable as expression of CD toxin B receptor was depleted in the FP + prebiotic group. Conclusion Supplementation with anti-inflammatory butyrate-supporting commensal bacteria and prebiotic may support innate immune responses and minimize bacterial burden and negative effects during antibiotic and CD exposure.

Protective Effect of Pediococcus pentosaceus LI05 Against Clostridium difficile Infection in a Mouse Model

“…To date, the standard laboratory investigations cannot distinguish between C. difficile colonization and true CDI in the fecal samples ( Bagdasarian et al, 2015 ). Further, previous studies of experimentally induced CDI focused on the inflammatory response in colonic tissues ( Pawlowski et al, 2010 ; Koon et al, 2016 ; Roychowdhury et al, 2018 ). Nevertheless, information regarding the inflammatory mediators circulating in the blood is still limited.…”

Barrier Protection and Recovery Effects of Gut Commensal Bacteria on Differentiated Intestinal Epithelial Cells In Vitro

“…R. intestinalis was able to increase the secretion of TGFβ in LPS-stimulated Caco-2 cells [87]. The in vivo application of live F. prausnitzii or the cell-free supernatant in experimental gut inflammation models attenuates the severity of inflammation and enhanced the intestinal epithelial barrier [32,68,86,88]. Similar effects have recently been demonstrated in a murine model of acute colitis for R. intestinalis [69].…”

The Microbiota–Gut–Brain Axis Heart Shunt Part I: The French Paradox, Heart Disease and the Microbiota

“…These prebiotics, in fact, may act synergistically to modify colonic and intestinal microbiota, which form a symbiosis and benefit human health [42]. In that regard, we found protective aspects of butyrate from the prebiotic potato starch with Faecalibacterium prausnitzii on Clostridium difficile infection and damage [43]. Others found prebiotic effects, using 16S rRNA pyrosequencing of the microbial DNA prepared from stool co-incubated with select fruits when fermented with feces from 10 donors [42].…”