PLoS Pathog:引发食物中毒的细菌或是克罗恩病发生的元凶

Acute Infectious Gastroenteritis Potentiates a Crohn’s Disease Pathobiont to Fuel Ongoing Inflammation in the Post-Infectious Period

来自麦克马斯特大学的研究人员近日通过研究发现，发生食物中毒后肠道中保留特殊细菌的人群或许在后期生活中患克罗恩病的风险会增加。相关研究刊登于国际杂志PLoS Pathogens上。利用克罗恩病小鼠模型研究者发现由常见食物中毒的细菌引发的急性感染性胃肠炎会加速黏附侵袭性大肠杆菌（AIEC）的生长。黏附侵袭性大肠杆菌常和克罗恩病相关。甚至在小鼠机体完全消除了食物中毒的细菌后。研究者仍然能够在其倡导中发现较高水平的AIEC。而AIEC的存在会在相当长一段时间内加剧小鼠的病情。

Crohn’s disease (CD) is a chronic inflammatory condition of diverse etiology. Exposure to foodborne pathogens causing acute gastroenteritis produces a long-term risk of CD well into the post-infectious period but the mechanistic basis for this ongoing relationship to disease onset is unknown. We developed two novel models to study the comorbidity of acute gastroenteritis caused by Salmonella Typhimurium or Citrobacter rodentium in mice colonized with adherent-invasive Escherichia coli (AIEC), a bacterial pathobiont linked to CD. Here, we show that disease activity in the post-infectious period after gastroenteritis is driven by the tissue-associated expansion of the resident AIEC pathobiont, with an attendant increase in immunopathology, barrier defects, and delays in mucosal restitution following pathogen clearance. These features required AIEC resistance to host defense peptides and a fulminant inflammatory response to the enteric pathogen. Our results suggest that individuals colonized by AIEC at the time of acute infectious gastroenteritis may be at greater risk for CD onset. Importantly, our data identify AIEC as a tractable disease modifier, a finding that could be exploited in the development of therapeutic interventions following infectious gastroenteritis in at-risk individuals. [ABSTRACT FROM AUTHOR]