Abstract
This study provides novel insight into the process by which surgical injury places the intestinal epithelium at risk for colonization by pathogenic microbes and impairment of its regenerative capacity via loss of its microbiota. We show that fecal transplant restores crypt homeostasis in association with repopulation of the microbiota within cecal crypts.
Highlights
NEW & NOTEWORTHY This study provides novel insight into the process by which surgical injury places the intestinal epithelium at risk for colonization by pathogenic microbes and impairment of its regenerative capacity via loss of its microbiota
In support of this latter hypothesis is the observation that intestinal stem cells produce the microbial pattern recognition receptors nucleotide-binding oligomerization domain-containing protein 2 (NOD2) and Toll-like receptor 4 (TLR4) [10, 19, 31] and that bacterial cell wall products can activate NOD2 in leucine-rich repeat-containing G protein-coupled receptor 5 (Lgr5)-positive stem cells and promote stem cell survival [20]
H&E staining (Fig. 1C) and fluorescence in situ hybridization (FISH) using a Texas red universal bacterial probe (Fig. 1, D and DЉ) demonstrated that most of the crypts were occupied by bacteria colonizing the full length of crypts (Fig. 1D=) including the base of crypts (Fig. 1DЉ)
Summary
NEW & NOTEWORTHY This study provides novel insight into the process by which surgical injury places the intestinal epithelium at risk for colonization by pathogenic microbes and impairment of its regenerative capacity via loss of its microbiota. We used a well-established model of lethal gutderived sepsis developed in our laboratory [1] and demonstrated that the process of surgery including preoperative starvation (S), preoperative antibiotic treatment (A), and a 30% hepatectomy (H) leads to depletion of microbiota within cecal crypt in association with altered crypt homeostasis as judged. Introduction of a fecal microbiota transplant (FMT) via enema in this model populated the cecal crypts with microbiota, prevented pathogen occupation, and maintained epithelial cell homeostasis as judged by stem cell proliferative capacity. Taken together, these findings define a role and spatial context in which the commensal microbiota within cecal crypts are involved in epithelial homeostasis
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