| セッション情報 |
Host-microbial Interaction and Immunology in IBD a. Basic Aspects
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| タイトル |
IF3a-1 Basic Aspects of IBD ： Overview of Host GeneticMicrobialDietary and Immunological Interactions
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| 演者 |
Ryan Balfour Sartor（University of North Carolina at Chapel HillUSA） |
| 共同演者 |
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| 抄録 |
Human Crohn’s disease and ulcerative colitis are chronicrelapsing inflammatory conditions that aremediated by abnormally aggressive T cell responses to a subset of normal commensal intestinal baeteriain genetically susceptible hosts． New insights into disease pathogenesis have been provided by an explo－sion of information in genetics and microbiology． Mechanistic studies in mouse models have demonstratedkey immune pathwaysidentified protective and aggressive bacterial species and demonstrated defectivemechanisms of IBD－related genes． A new concept for pathQgenesis of a su／bset of Crohn’s disease patientsis that genetic defects in innate immune kiMng of bacteria results in compensatory activation of THI andTH17 cells that respond to bacterial antigens． This is relevant to function of NOD2ATG16L l and IRGM inCrohn’s disease． Gnotobiotic rodent studies demonstrate that normal commensal bacteria are required forinduction of chronicT cell mediated colitis ； that a subset of normal intestinal bacteria are protectivewhile others cause disease ； that each host can respond differently to different bacteria ； and in the samehost different bacteria can induce disease in different intestinal regions． Recent data indicate that individ－ual bacteria and even defined bacterial components can activate IBD related immune pathwaysfor exam－ple segn tental filamentous bacteria （SFB） activate IL－23 and IL－17 cellswhile Clostridium subsets andpolysaccharide A of Bacteroides fragilis can activate regulatory T cells． Finallydietary components canalter intestinal b acterial profilesinfluence bacterial metabolism and stimulate immune pathways． For ex－amplenonabsorbed fiber can be metabolized to short chain fatty acids such as butyrateand Vit A （reti－noic acid） can induce Treg cells． Thusgeneticmicrobialenvironmental and immunologic factors interactto determine mucosal homeostasis or inflammation． |
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