Pothoulakis C
Division of Gastroenterology, Beth Israel Hospital, Harvard Medical School, Boston, MA, USA.
Eur J Gastroenterol Hepatol. 1996 Nov;8(11):1041-7. doi: 10.1097/00042737-199611000-00003.
Clostridium difficile is now regarded as a major enteric pathogen in hospitals and nursing-home facilities. The pathophysiology of this pathogen involves alterations of the indigenous colonic flora by antibiotics, ingestion of spores and colonization by C. difficile, followed by release of its toxins. Although most of the research on the intestinal effects of C. difficile had been focused on its enterotoxin or toxin A, recent results indicate that toxin B, the cytotoxin of C. difficile, is also active in human colon. The cloning and sequencing of the toxin A and toxin B gene and the identification of the GTP-binding protein Rho as their intracellular target represent major advances in our understanding of the mode of action of these toxins. An important characteristic of C. difficile infection is the dramatic inflammation seen in pseudomembranous colitis. Recent studies indicate that an interplay between lamina propria neuroimmune cells and intestinal epithelial cells may be central in pathogenesis of this toxin-mediated inflammatory response.
艰难梭菌现在被认为是医院和疗养院设施中的一种主要肠道病原体。这种病原体的病理生理学涉及抗生素对肠道固有菌群的改变、艰难梭菌孢子的摄入和定植，随后释放其毒素。尽管大多数关于艰难梭菌肠道效应的研究都集中在其肠毒素或毒素A上，但最近的结果表明，艰难梭菌的细胞毒素毒素B在人类结肠中也具有活性。毒素A和毒素B基因的克隆和测序以及将GTP结合蛋白Rho鉴定为它们的细胞内靶点，代表了我们对这些毒素作用模式理解的重大进展。艰难梭菌感染的一个重要特征是在假膜性结肠炎中可见的剧烈炎症。最近的研究表明，固有层神经免疫细胞和肠道上皮细胞之间的相互作用可能是这种毒素介导的炎症反应发病机制的核心。
