坚守杏坛 http://www.changfengzx.com/cfxjj/7326.html摘要：
Theprecisemechanismbywhichoralinfectioncontributestothepathogenesisofextra-oraldiseasesremainsunclear.Here,wereportthatperiodontalinflammationexacerbatesgutinflammationinvivo.Periodontitisleadstoexpansionoforalpathobionts,includingKlebsiellaandEnterobacterspecies,intheoralcavity.Amassedoralpathobiontsareingestedandtranslocatetothegut,wheretheyactivatetheinflammasomeincolonicmononuclearphagocytes,triggeringinflammation.Inparallel,periodontitisresultsingenerationoforalpathobiont-reactiveTh17cellsintheoralcavity.Oralpathobiont-reactiveTh17cellsareimprintedwithguttropismandmigratetotheinflamedgut.Wheninthegut,Th17cellsoforalorigincanbeactivatedbytranslocatedoralpathobiontsandcausedevelopmentofcolitis,buttheyarenotactivatedbygut-residentmicrobes.Thus,oralinflammation,suchasperiodontitis,exacerbatesgutinflammationbysupplyingthegutwithbothcolitogenicpathobiontsandpathogenicTcells.
口腔感染导致口腔外疾病发病机理的确切机制尚不清楚。在这里，我们报告牙周炎症在体内加剧了肠道炎症反应。牙周炎导致口腔中包括克雷伯菌和肠杆菌种在内的口腔病原菌的扩增。口腔内菌群可转移至肠道，在那里它们激活结肠单核吞噬细胞中的炎症小体，从而引发炎症。同时，牙周炎导致在口腔中产生口腔病原体反应性Th17细胞。口腔病原体反应性Th17细胞可迁移至出现炎症的肠道。当进入肠道时，口腔起源的Th17细胞可被易位的口腔致病菌激活并引起结肠炎的发展，但不会被肠道内的微生物激活。因此，口腔炎症，例如牙周炎，通过向肠道供应致病性致病菌和致病性T细胞，加剧了肠道炎症反应。
文章来源：Kitamoto,S.,Nagao-Kitamoto,H.,Jiao,Y.,Gillilland,M.G.,Hayashi,A.,Imai,J.,…Kamada,N.().TheIntermucosalConnectionbetweentheMouthandGutinCommensalPathobiont-DrivenColitis.Cell.doi:10./j.cell..05.
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