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作 者:陈烨[1] 林倩云 CHEN Ye LIN Qianyun(Department of Gastroenterology, Nanfang Hospital, Southern Medical University, Guangdong Provincial Key Laboratory of Gastroenterology, Guangzhou (510515)
机构地区:[1]南方医科大学附属南方医院消化内科,广东省胃肠实验重点实验室,510515
出 处:《胃肠病学》2017年第7期385-389,共5页Chinese Journal of Gastroenterology
摘 要:艰难梭菌(C.difficile)是院内获得性腹泻和伪膜性肠炎的首要病原体,产毒菌株主要通过产生毒素A和毒素B引起腹泻、肠道炎症甚至肠坏死。有研究表明,C.difficile在体内的产毒水平是影响C.difficile相关性疾病(CDAD)临床表型的重要因素,而细菌毒素与临床表型的具体联系尚不明确。本文主要针对CDAD临床表型以及毒素蛋白的结构、功能及其调控等方面进行论述,探讨细菌毒素与临床表型的关系,为进一步深入研究C.difficile的致病机制并探索新的药物治疗靶点奠定理论基础。Clostridium difficile (C. difficile ) infection is the leading cause of hospital-acquired diarrhea and pseudomembranous colitis. C. dijficile-associated disease (CDAD) is mediated mainly by two bacterial toxins, TcdA and TcdB, which cause the diarrhea, as well as colitis and even intestinal necrosis. It has been indicated that level of C. difftcile toxin is an important factor influencing the clinical phenotype of CDAD, however, the exact association between toxin and clinical phenotype remains unclear. In this article, we summarized the clinical phenotype of CDAD, the structure, function and regulatory mechanism of C. difficile toxin and discussed the relationship between C. difficile toxin and clinical phenotype, which may help to understand the pathogenic mechanism and provide possible therapeutic target for C. difftcile infection.
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