Nottingham Digestive Diseases Centre, Biomedical Research Unit, University Hospital, Nottingham, UK.
Dig Dis. 2009;27 Suppl 1:48-54. doi: 10.1159/000268121. Epub 2010 Mar 4.
While recent studies have indicated that the colonic mucosa in irritable bowel syndrome (IBS) shows an increase in inflammatory cells, this 'inflammation' is quantitatively less than in inflammatory bowel disease (IBD) and of a different nature with a predominance of mast cells, particularly in female patients. Inflammation can arise via numerous pathways including infection, stress, food allergy and changes in gut microbiota. Low-grade mucosal inflammation throughout the colon and including the terminal ileum can be seen for many months after an attack of acute gastroenteritis and is a feature of post-infective IBS. Measurements of gut permeability also show a prolonged increase in both the small and large bowel in both post-infective IBS and IBS with diarrhoea predominance. This has been linked to visceral hypersensitivity, but whether this is causal or an epiphenomenon remains uncertain. Studying the risk factors for post-infective IBS has shown the importance of both local and microbiological factors, as well as psychological factors, including adverse life events, anxiety and depression. Stress in both animals and humans can activate mast cells, which (by increasing gut permeability) may allow activation of the systemic immune system. Demonstration of the importance of the low-grade inflammation observed awaits definitive large scale trials of agents designed to specifically reverse these changes.
虽然最近的研究表明，肠易激综合征（IBS）的结肠黏膜中炎症细胞增多，但这种“炎症”在数量上少于炎症性肠病（IBD），且性质不同，以肥大细胞为主，尤其是在女性患者中。炎症可以通过多种途径引起，包括感染、应激、食物过敏和肠道微生物群的变化。急性胃肠炎发作后数月，整个结肠甚至末端回肠都可能出现低级别黏膜炎症，这是感染后肠易激综合征的一个特征。肠道通透性的测量也显示，感染后肠易激综合征和腹泻为主的肠易激综合征患者的小肠和大肠通透性均持续增加。这与内脏高敏有关，但这是否是因果关系或继发现象仍不确定。研究感染后肠易激综合征的危险因素表明，局部和微生物因素以及心理因素（包括不良生活事件、焦虑和抑郁）都很重要。动物和人类的压力都可以激活肥大细胞，这可能会增加肠道通透性，从而激活全身免疫系统。观察到的低度炎症的重要性有待于专门设计用于逆转这些变化的药物的大规模临床试验来证实。
