Metabolic syndrome is a group of obesity-related metabolic abnormalities that increase an individual's risk of developing type 2 diabetes and cardiovascular disease. Here, we show that mice ...genetically deficient in Toll-like receptor 5 (TLR5), a component of the innate immune system that is expressed in the gut mucosa and that helps defend against infection, exhibit hyperphagia and develop hallmark features of metabolic syndrome, including hyperlipidemia, hypertension, insulin resistance, and increased adiposity. These metabolic changes correlated with changes in the composition of the gut microbiota, and transfer of the gut microbiota from TLR5-deficient mice to wild-type germ-free mice conferred many features of metabolic syndrome to the recipients. Food restriction prevented obesity, but not insulin resistance, in the TLR5-deficient mice. These results support the emerging view that the gut microbiota contributes to metabolic disease and suggest that malfunction of the innate immune system may promote the development of metabolic syndrome.
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BFBNIB, NMLJ, NUK, PNG, SAZU, UL, UM, UPUK
Gut mucosal barrier breakdown and inflammation have been associated with high levels of flagellin, the principal bacterial flagellar protein. Although several gut commensals can produce flagella, ...flagellin levels are low in the healthy gut, suggesting the existence of control mechanisms. We find that mice lacking the flagellin receptor Toll-like receptor 5 (TLR5) exhibit a profound loss of flagellin-specific immunoglobulins (Igs) despite higher total Ig levels in the gut. Ribotyping of IgA-coated cecal microbiota showed Proteobacteria evading antibody coating in the TLR5−/− gut. A diversity of microbiome members overexpressed flagellar genes in the TLR5−/− host. Proteobacteria and Firmicutes penetrated small intestinal villi, and flagellated bacteria breached the colonic mucosal barrier. In vitro, flagellin-specific Ig inhibited bacterial motility and downregulated flagellar gene expression. Thus, innate-immunity-directed development of flagellin-specific adaptive immune responses can modulate the microbiome’s production of flagella in a three-way interaction that helps to maintain mucosal barrier integrity and homeostasis.
•TLR5−/− mice have reduced levels of anti-flagellin antibodies in the gut•Flagella-related genes of commensal microbes are upregulated in TLR5−/− mouse guts•Antibodies against flagellin induce downregulation of flagella genes•Flagellated bacteria penetrate TLR5−/− small intestinal villi and mucosal barrier
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
Colitis results from breakdown of homeostasis between intestinal microbiota and the mucosal immune system, with both environmental and genetic influencing factors. Flagellin receptor TLR5-deficient ...mice (T5KO) display elevated intestinal proinflammatory gene expression and colitis with incomplete penetrance, providing a genetically sensitized system to study the contribution of microbiota to driving colitis. Both colitic and noncolitic T5KO exhibited transiently unstable microbiotas, with lasting differences in colitic T5KO, while their noncolitic siblings stabilized their microbiotas to resemble wild-type mice. Transient high levels of proteobacteria, especially enterobacteria species including E. coli, observed in close proximity to the gut epithelium were a striking feature of colitic microbiota. A Crohn’s disease-associated E. coli strain induced chronic colitis in T5KO, which persisted well after the exogenously introduced bacterial species had been eliminated. Thus, an innate immune deficiency can result in unstable gut microbiota associated with low-grade inflammation, and harboring proteobacteria can drive and/or instigate chronic colitis.
► TLR5-deficient mice (T5KO) are prone to develop postweaning gut inflammation ► Colitic T5KO are associated with increased microbial volatility and proteobacteria ► T5KO show increased susceptibility to Crohn’s disease-associated E. coli (AIEC) ► AIEC persists longer in T5KO and induces chronic intestinal inflammation
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
We tested the role of hydrodynamics in the use of chemical signals by the red swamp crayfish (Procambarus clarkii). We conditioned the crayfish in either a still water or flowing water habitat for 2 ...weeks. We then observed the crayfish in control (no stimulus) and experimental (food stimulus) trials in one of two flowing water habitats-laminar or turbulent. Habitat use was significantly different between control and experimental observations, but there was no effect of conditioning habitat or experimental habitat on the responses to the food stimulus. This study adds to a growing body of literature consistent with the idea that gross responses to chemical stimuli in crayfish are not affected by the hydrodynamic context in which they are encountered.
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BFBNIB, DOBA, GIS, IJS, IZUM, KILJ, KISLJ, NUK, PILJ, PNG, SAZU, UILJ, UKNU, UL, UM, UPUK
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