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Title Interplay Between Microbiota, Chronic Gut Inflammation and Metabolic Disease

Presented by Matam Vijay-Kumar, Ph.D. Assistant Professor Center for Inflammation, Immunity & Infection Department of Biology Georgia State University Petit Science Center

Toll LIke Receptor 5 (TLR5), an innate immune receptor expressed basolaterally by epithelial cells in multiple tissues, detects bacterial flagellin and serves to minitor and maintain the barrier between the lumen and host tissue. TLR5's function is especially important in the gut, where it works in concert with other pattern recognition receptors to protect against pathogenic and opportunistic bacertia. Mice lacking TLR5 (TLR5KO) are predisposed to developing spontaneious robust i nflammation resulting in colitis, which is TLR4 and microbiota dependent. In addition, non-colitic TLR5KO mice exhibit symptoms of metabolic syndrome such as obesity, insulin resistance, hyperlipidemia and hypertension. High-fat diet aggravates where as calorie restriction and broad-spectrum antibiotics prevents metabolic syndrome in TLR5KO mice. Interestingly, altered cecal microbiota from TLR5KO mice is sufficient to transfer fetabolic syndrome to germ free WT mice. Accordingly, germ free TLR5KO mice are free from colitis and metabolic syndrome. Collectively, our study demonstrates that low-grade chronic intestinal inflammation can result in metabolic syndrome.