Host-microbial Cross-talk in Inflammatory Bowel Disease

Abstract

A vast community of commensal microorganisms, commonly referred to as the gut microbiota, colonizes the gastrointestinal tract (GI). The involvement of the gut microbiota in the maintenance of the gut ecosystem is two-fold: it educates host immune cells and protects the host from pathogens. However, when healthy microbial composition and function are disrupted (dysbiosis), the dysbiotic gut microbiota can trigger the initiation and development of various GI diseases, including inflammatory bowel disease (IBD). IBD, primarily includes ulcerative colitis (UC) and Crohn's disease (CD), is a major global public health problem affecting over 1 million patients in the United States alone. Accumulating evidence suggests that various environmental and genetic factors contribute to the pathogenesis of IBD. In particular, the gut microbiota is a key factor associated with the triggering and presentation of disease. Gut dysbiosis in patients with IBD is defined as a reduction of beneficial commensal bacteria and an enrichment of potentially harmful commensal bacteria (pathobionts). However, as of now it is largely unknown whether gut dysbiosis is a cause or a consequence of IBD. Recent technological advances have made it possible to address this question and investigate the functional impact of dysbiotic microbiota on IBD. In this review, we will discuss the recent advances in the field, focusing on host-microbial cross-talk in IBD.

Six‐Week High‐Fat Diet Alters the Gut Microbiome and Promotes Cecal Inflammation, Endotoxin Production, and Simple Steatosis without Obesity in Male Rats

“…Solka Floc is a powdered cellulose added to dry pet food for shape and texture. Cellulose acts as an energy source for Actinobacteria , which produces short‐chain fatty acids responsible for anti‐inflammatory properties (Nagao‐Kitamoto and Kamada, ). This amount of fiber was greater than the cellulose and lignin content reported for the chow diet (3.5%).…”

Liver X Receptor regulates Th17 and RORγt+ Treg cells by distinct mechanisms

“…In these experiments, we observed significantly higher enrichment of bacteria belonging to the family Ruminococcaceae and Lachnospiraceae in LXRα −/− mice compared to WT littermates in steady state, suggesting that lack of LXRα allows preferential colonization of specific groups of bacteria. Both Ruminococcaceae and Lachnospiraceae belong to the order Clostridiales and phylum Firmicutes and have been associated with multiple human diseases including IBD 22-24 and atherosclerosis 25,26 . While the abundance of both Ruminococcaceae and Lachnospiraceae are decreased in IBD patients, suggesting a protective role, they have been shown to be associated with pro-atherogenic effects.…”

BowSaw: inferring higher-order trait interactions associated with complex biological phenotypes

“…Of the five associated taxa, we 497 suspect that the absence of lachnospira, lachnospiracea UCG 001, and tyzzerella are 498 biologically meaningful. We have reason to believe so because it has been reported that 499 the lachnospiraceae family is generally suppressed in Crohn's disease [32][33][34]. 500…”