Alterations of Gut Bacteria in Hirschsprung Disease and Hirschsprung-Associated Enterocolitis

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Abstract

Hirschsprung-associated enterocolitis (HAEC) is a common life-threatening complication of Hirschsprung disease (HSCR). It has been proposed that gut microbiota, which have an essential role in gut-homeostasis, are associated with HAEC. Recent studies demonstrated an increase in alpha diversity of fecal microbiota over time in HSCR mice and a decrease in diversity after surgery. In addition, clinical studies have reported a reduction in bacterial richness in HSCR children after surgery. Some studies revealed a difference in microbiota between the proximal ganglionic and distal aganglionic intestine and found a difference in bacterial character between fecal and colonic specimens. HAEC studies found an increase in Proteobacteria, especially Escherichia and Enterobacteriaceae, with a decrease in Firmicutes and Bifidobacterium in HAEC patients. However, the direction of alpha diversity in HAEC patients is still controversial. The self-comparison of microbiota in treatment periods suggested that probiotics might improve gut dysbiosis and decrease the frequency of enterocolitis, but some reported contradictory findings. This review comprehensively summarizes and discusses key findings from animal and clinical data of the distinct microbiome associated with HCSR and the association of gut dysbiosis with the development of HAEC. This information should be useful in the establishment of novel interventions to improve gut dysbiosis and prevent enterocolitis in HSCR patients.

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Proteobacteria: microbial signature of dysbiosis in gut microbiota.

Na-Ri Shin, Tae Whon, Jin-Woo Bae (2015)

Recent advances in sequencing techniques, applied to the study of microbial communities, have provided compelling evidence that the mammalian intestinal tract harbors a complex microbial community whose composition is a critical determinant of host health in the context of metabolism and inflammation. Given that an imbalanced gut microbiota often arises from a sustained increase in abundance of the phylum Proteobacteria, the natural human gut flora normally contains only a minor proportion of this phylum. Here, we review studies that explored the association between an abnormal expansion of Proteobacteria and a compromised ability to maintain a balanced gut microbial community. We also propose that an increased prevalence of Proteobacteria is a potential diagnostic signature of dysbiosis and risk of disease.

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Dysfunction of the intestinal microbiome in inflammatory bowel disease and treatment

Xochitl C Morgan, Timothy Tickle, Harry Sokol … (2012)

Background The inflammatory bowel diseases (IBD) Crohn's disease and ulcerative colitis result from alterations in intestinal microbes and the immune system. However, the precise dysfunctions of microbial metabolism in the gastrointestinal microbiome during IBD remain unclear. We analyzed the microbiota of intestinal biopsies and stool samples from 231 IBD and healthy subjects by 16S gene pyrosequencing and followed up a subset using shotgun metagenomics. Gene and pathway composition were assessed, based on 16S data from phylogenetically-related reference genomes, and associated using sparse multivariate linear modeling with medications, environmental factors, and IBD status. Results Firmicutes and Enterobacteriaceae abundances were associated with disease status as expected, but also with treatment and subject characteristics. Microbial function, though, was more consistently perturbed than composition, with 12% of analyzed pathways changed compared with 2% of genera. We identified major shifts in oxidative stress pathways, as well as decreased carbohydrate metabolism and amino acid biosynthesis in favor of nutrient transport and uptake. The microbiome of ileal Crohn's disease was notable for increases in virulence and secretion pathways. Conclusions This inferred functional metagenomic information provides the first insights into community-wide microbial processes and pathways that underpin IBD pathogenesis.

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Changes in gut microbiota control inflammation in obese mice through a mechanism involving GLP-2-driven improvement of gut permeability

P D Cani, S Possemiers, T Van de Wiele … (2009)

Background and aims: Obese and diabetic mice display enhanced intestinal permeability and metabolic endotoxaemia that participate in the occurrence of metabolic disorders. Our recent data support the idea that a selective increase of Bifidobacterium spp. reduces the impact of high-fat diet-induced metabolic endotoxaemia and inflammatory disorders. Here, we hypothesised that prebiotic modulation of gut microbiota lowers intestinal permeability, by a mechanism involving glucagon-like peptide-2 (GLP-2) thereby improving inflammation and metabolic disorders during obesity and diabetes. Methods: Study 1: ob/ob mice (Ob-CT) were treated with either prebiotic (Ob-Pre) or non-prebiotic carbohydrates as control (Ob-Cell). Study 2: Ob-CT and Ob-Pre mice were treated with GLP-2 antagonist or saline. Study 3: Ob-CT mice were treated with a GLP-2 agonist or saline. We assessed changes in the gut microbiota, intestinal permeability, gut peptides, intestinal epithelial tight-junction proteins ZO-1 and occludin (qPCR and immunohistochemistry), hepatic and systemic inflammation. Results: Prebiotic-treated mice exhibited a lower plasma lipopolysaccharide (LPS) and cytokines, and a decreased hepatic expression of inflammatory and oxidative stress markers. This decreased inflammatory tone was associated with a lower intestinal permeability and improved tight-junction integrity compared to controls. Prebiotic increased the endogenous intestinotrophic proglucagon-derived peptide (GLP-2) production whereas the GLP-2 antagonist abolished most of the prebiotic effects. Finally, pharmacological GLP-2 treatment decreased gut permeability, systemic and hepatic inflammatory phenotype associated with obesity to a similar extent as that observed following prebiotic-induced changes in gut microbiota. Conclusion: We found that a selective gut microbiota change controls and increases endogenous GLP-2 production, and consequently improves gut barrier functions by a GLP-2-dependent mechanism, contributing to the improvement of gut barrier functions during obesity and diabetes.