Francés Rubén, González-Navajas José M, Zapater Pedro, Muñoz Carlos, Caño Rocío, Pascual Sonia, Márquez Dorkas, Santana Francia, Pérez-Mateo Miguel, Such José
CIBERehd, Instituto de Salud Carlos III, Madrid, Spain.
J Clin Immunol. 2007 Jul;27(4):438-44. doi: 10.1007/s10875-007-9090-2. Epub 2007 Apr 3.
Translocation of intestinal bacteria to ascitic fluid is, probably, the first step in the development of spontaneous bacterial peritonitis in patients with cirrhosis. Proteins of the complement system are soluble mediators implicated in the host immune response to bacterial infections and its activation has been traditionally considered to be an endotoxin-induced phenomenon. The aim of this study was to compare the modulation of these proteins in response to the presence of bacterial DNA and/or endotoxin in patients with advanced cirrhosis and ascites in different clinical conditions. Groups I and II consisted of patients without/with bacterial DNA. Group III included patients with spontaneous bacterial peritonitis and Group IV with patients receiving norfloxacin as secondary long-term prophylaxis of spontaneous bacterial peritonitis. Serum and ascitic fluid levels of endotoxin and truncated residues of the complement system were measured by ELISA. The complement system is triggered in response to bacterial DNA, as evidenced by significantly increased levels of C3b, membrane attack complex, and C5a in patients from Groups II and III compared with patients without bacterial DNA (Group I) and those receiving norfloxacin (Group IV). Gram classification did not further differentiate the immune response between patients within groups II and III, even though endotoxin levels were, as expected, significantly higher in patients with bacterial DNA from gram-negative microorganisms. The complement protein activation observed in patients with bacterial DNA in blood and ascitic fluid is indistinguishable from that observed in patients with spontaneous bacterial peritonitis and may occur in an endotoxin-independent manner.
肠道细菌易位至腹水可能是肝硬化患者自发性细菌性腹膜炎发生过程中的第一步。补体系统的蛋白质是参与宿主对细菌感染免疫反应的可溶性介质，其激活传统上被认为是内毒素诱导的现象。本研究的目的是比较晚期肝硬化腹水患者在不同临床情况下，细菌DNA和/或内毒素存在时这些蛋白质的调节情况。第一组和第二组由无/有细菌DNA的患者组成。第三组包括自发性细菌性腹膜炎患者，第四组为接受诺氟沙星作为自发性细菌性腹膜炎二级长期预防的患者。通过酶联免疫吸附测定法检测血清和腹水内毒素水平以及补体系统的截短片段。补体系统因细菌DNA而被激活，与无细菌DNA的患者（第一组）和接受诺氟沙星治疗的患者（第四组）相比，第二组和第三组患者的C3b、膜攻击复合物和C5a水平显著升高即证明了这一点。革兰氏分类法并未进一步区分第二组和第三组患者之间的免疫反应，尽管正如预期的那样，来自革兰氏阴性微生物且有细菌DNA的患者内毒素水平显著更高。在血液和腹水中有细菌DNA的患者中观察到的补体蛋白激活与自发性细菌性腹膜炎患者中观察到的情况无法区分，并且可能以内毒素非依赖的方式发生。
