Papamichael Konstantinos, Konstantopoulos Panagiotis, Mantzaris Gerassimos J
Konstantinos Papamichael, Panagiotis Konstantopoulos, Gerassimos J Mantzaris, First Gastroenterology Clinic, Evaggelismos Hospital, 10676 Athens, Greece.
World J Gastroenterol. 2014 Jun 7;20(21):6374-85. doi: 10.3748/wjg.v20.i21.6374.
Helicobacter pylori (H. pylori) infection is one of the most widely spread infectious diseases in humans. It can cause chronic gastritis, peptic ulcer disease and gastric malignancies and has been associated with extra-gastric disorders. H. pylori elicit a chronic systemic inflammatory response which, under certain conditions, may trigger autoimmune reactions and may be implicated in the pathogenesis of autoimmune diseases. Although the pathogenesis of inflammatory bowel disease (IBD) is unknown, it is thought to result from complex interactions between environmental factors and microbiota in the gut of individuals who are genetically susceptible. Several bacterial and viral agents have been implicated in the aetiology of IBD. In theory, H. pylori infection could be involved in the pathogenesis of IBD by inducing alterations in gastric and/or intestinal permeability or by causing immunological derangements resulting in absorption of antigenic material and autoimmunity via various immunological pathways. Similar mechanisms may also be responsible for the co-existence of IBD with other autoimmune diseases and/or extra-intestinal manifestations. However, the epidemiological data fail to support this association. In fact, various studies indicate that the prevalence of H. pylori infection is low in patients with IBD, suggesting a protective role for this infection in the development of IBD. In this report, we aim to shed light on proposed mechanisms and confounding factors underlying the potential link between H. pylori infection and IBD.
幽门螺杆菌(H. pylori)感染是人类中传播最广泛的传染病之一。它可导致慢性胃炎、消化性溃疡疾病和胃部恶性肿瘤,并与胃外疾病有关。幽门螺杆菌引发慢性全身性炎症反应,在某些情况下,可能引发自身免疫反应,并可能与自身免疫性疾病的发病机制有关。虽然炎症性肠病(IBD)的发病机制尚不清楚,但人们认为它是由环境因素与肠道微生物群在具有遗传易感性个体的肠道中复杂相互作用导致的。几种细菌和病毒因子被认为与IBD的病因有关。理论上,幽门螺杆菌感染可能通过诱导胃和/或肠道通透性改变,或通过引起免疫紊乱,导致抗原物质吸收和经由各种免疫途径的自身免疫,从而参与IBD的发病机制。类似机制也可能是IBD与其他自身免疫性疾病和/或肠外表现并存的原因。然而,流行病学数据并不支持这种关联。事实上,各种研究表明,IBD患者中幽门螺杆菌感染的患病率较低,提示这种感染在IBD发生过程中具有保护作用。在本报告中,我们旨在阐明幽门螺杆菌感染与IBD之间潜在联系的提出机制和混杂因素。