Malchow H A
Klinikum Leverkusen, Medizinische Klinik 2, Germany.
J Clin Gastroenterol. 1997 Dec;25(4):653-8. doi: 10.1097/00004836-199712000-00021.
Involvement of pathogenic or potentially pathogenic bacteria in the pathogenesis of inflammatory bowel disease has long been suggested because, among other reasons, the inflammatory response resembles that in infectious bowel diseases. Elevated antibody levels to pathogen antigens and a changed metabolic activity of the intestinal microflora have been detected in patients with Crohn's disease. Several studies have revealed a possible etiologic link between intestinal microorganisms and inflammatory bowel disease. Therefore, several therapeutic strategies, including reduction or dilution of bacterial components in the intestine by antibiotics or intestinal lavage, respectively, inactivation of inflammatory bacterial products, and reconstitution of intestinal microflora have been employed, substantiating the idea that dysfunction of the intestinal mucosal barrier and an alteration of bacterial composition contribute to the inflammatory disease. However, the beneficial effect of restoration of the physiologic intestinal microflora in colonic inflammation by exogenous administration of a viable nonpathogenic bacterium has not been investigated before in a placebo-controlled study. Promising results came from the present pilot study in which the nonpathogenic Escherichia coli strain Nissle 1917 was tested for efficacy and tolerance in maintaining remission in patients with colonic Crohn's disease. Application of the physiologic bacteria reduced the risk for relapse and minimized the need for glucocorticoids. Therefore we are convinced that in Crohn's disease parts of the intestinal microflora, including the host's immune response toward indigenous flora or an impairment of the gut flora's metabolic activity are involved in the development or at least in the onset of relapse from remissive of colonic Crohn's disease. However, more data are necessary to prove the benefit of E. coli strain Nissle 1917 as a new therapy to maintain remission of colonic Crohn's disease.
长期以来，人们一直认为致病性或潜在致病性细菌参与了炎症性肠病的发病机制，原因之一是炎症反应与感染性肠病相似。在克罗恩病患者中检测到针对病原体抗原的抗体水平升高以及肠道微生物群代谢活性改变。多项研究揭示了肠道微生物与炎症性肠病之间可能的病因联系。因此，人们采用了多种治疗策略，包括分别使用抗生素或肠道灌洗来减少或稀释肠道中的细菌成分、使炎性细菌产物失活以及重建肠道微生物群，这证实了肠道黏膜屏障功能障碍和细菌组成改变会导致炎症性疾病的观点。然而，在安慰剂对照研究中，此前尚未研究过通过外源性给予活的非致病性细菌来恢复生理性肠道微生物群对结肠炎症的有益作用。本初步研究取得了有前景的结果，其中对非致病性大肠杆菌菌株Nissle 1917在维持结肠克罗恩病患者缓解方面的疗效和耐受性进行了测试。应用生理性细菌降低了复发风险，并减少了对糖皮质激素的需求。因此，我们确信在结肠克罗恩病中，肠道微生物群的某些部分，包括宿主对本土菌群的免疫反应或肠道菌群代谢活性受损，参与了疾病的发展，或者至少参与了缓解期结肠克罗恩病复发的起始。然而，需要更多数据来证明大肠杆菌菌株Nissle 1917作为维持结肠克罗恩病缓解的新疗法的益处。
