Host-Mediated Inflammation Disrupts the Intestinal Microbiota and Promotes the Overgrowth of Enterobacteriaceae

Abstract

While the normal microbiota has been implicated as a critical defense against invading pathogens, the impact of enteropathogenic infection and host inflammation on intestinal microbial communities has not been elucidated. Using mouse models of Citrobacter rodentium, which closely mimics human diarrheal pathogens inducing host intestinal inflammation, and Campylobacter jejuni infection, as well as chemically and genetically induced models of intestinal inflammation, we demonstrate that host-mediated inflammation in response to an infecting agent, a chemical trigger, or genetic predisposition markedly alters the colonic microbial community. While eliminating a subset of indigenous microbiota, host-mediated inflammation supported the growth of either the resident or introduced aerobic bacteria, particularly of the Enterobacteriaceae family. Further, assault by an enteropathogen and host-mediated inflammation combined to significantly reduce the total numbers of resident colonic bacteria. These findings underscore the importance of intestinal microbial ecosystems in infectious colitis and noninfectious intestinal inflammatory conditions, such as inflammatory bowel disease.

Nutrition, intestinal defence and the microbiome

“…Antibiotics can have longlasting effects on the microbiota; deep sequencing of the microbiome from three adults before and after ciprofloxacin treatment has shown that most taxa recover by 4 weeks, but some taxa take much longer to recover (13) . Similar results have been obtained in mice (14) , in which it has also been shown that an intestinal pathogen (in this case Citrobacter rodentium) perturbs the microbiota but the pretreatment status quo returns within 28 d (15) . Importantly, the microbiome tends to recover a composition characteristic of that individual even after treatment with a broad spectrum antibiotic, despite the apparent opportunity that this treatment represents for a change in the flora and that is sometimes exploited by Clostridium difficile (16) .…”

Enterococcus faecalis from newborn babies regulate endogenous PPARγ activity and IL-10 levels in colonic epithelial cells

“…Selective species of E. faecalis have been shown to antagonize diarrhea induced by E. coli K88 through unknown mechanisms (32), but it is conceivable that not all strains of E. faecalis will have beneficial effects. Moreover, it was recently shown that the intestinal ecosystem is altered in cases of inflammatory reaction to stimuli in the host (33). Importantly, the composition of the microbiota is restored after dissipation of the inflammatory signal, a feature of a healthy homeostatic mechanism.…”

Gut inflammation can boost horizontal gene transfer between pathogenic and commensal Enterobacteriaceae

“…or pathogenic E. coli strains can suppress the anaerobic microbiota and boost enterobacterial colonization densities (20)(21)(22)(23)(24). Here, we show that disease-triggered enterobacterial blooms can fuel HGT between two prominent members of this family, Salmonella enterica serovar Typhimurium (S. Tm) and E. coli.…”