Unidad Hepática, Hospital General Universitario, Avda. Pintor Baeza 12, 03010, Alicante, Spain.
J Mol Med (Berl). 2010 May;88(5):487-95. doi: 10.1007/s00109-009-0582-9. Epub 2010 Jan 20.
Bacterial translocation in patients with cirrhosis induces a marked proinflammatory activity that may be different against viable bacteria or bacterial products. The aim of this study is to identify new markers of bacterial translocation by investigating bacterial-driven peptides and correlate their presence with the inflammatory response. Patients with cirrhosis and ascites were included. An analysis by two-dimensional polyacrylamide gel electrophoresis of ascitic fluid total protein from patients (n = 47) and from frequently detected bacterial strains was performed. Two-dimensional maps were digitally compared. The identification of possible markers was performed by mass spectrometry. TNF-alpha, IFN-gamma, IL-12, nitric oxide, and proteins of the complement and lipopolysaccharide-binding protein levels were measured in ascitic fluid samples of patients by enzyme-linked immunosorbent assay. Patients were distributed according to the presence (group I, n = 16) and absence (group II, n = 31) of serum and ascitic fluid bacterial DNA. Among clinical and analytical differences between groups, only mean arterial pressure was significantly higher in patients from group II. Identified bacterial peptides were associated with bacterial protection against immune defenses and included glyceraldehyde-3-phosphate dehydrogenase A, Porin OmpC, and HSP60. Eight patients from group I also showed bacterial peptides, whereas none from group II did. All studied mediators of immune activation were significantly higher in patients with bacterial DNA than in patients without bacterial DNA. TNF-alpha, IFN-gamma, and proteins of the complement were significantly increased in patients with bacterial peptides versus those without bacterial peptides. Bacterial peptide translocation is present in the ascitic fluid of a subgroup of patients with advanced cirrhosis and is associated with an increased immune response.
肝硬化患者的细菌易位会引起明显的促炎活性，这种活性可能针对活细菌或细菌产物而有所不同。本研究的目的是通过研究细菌驱动肽来确定新的细菌易位标志物，并将其与炎症反应相关联。纳入肝硬化伴腹水的患者。对患者（n=47）和经常检测到的细菌菌株的腹水总蛋白进行二维聚丙烯酰胺凝胶电泳分析。对二维图谱进行数字比较。通过质谱法进行可能标志物的鉴定。通过酶联免疫吸附试验测量患者腹水样本中的 TNF-α、IFN-γ、IL-12、一氧化氮以及补体和脂多糖结合蛋白的蛋白质水平。根据患者血清和腹水细菌 DNA 的存在（I 组，n=16）和不存在（II 组，n=31）对患者进行分组。在两组间的临床和分析差异中，仅 II 组患者的平均动脉压显著更高。鉴定出的细菌肽与细菌对免疫防御的保护有关，包括甘油醛-3-磷酸脱氢酶 A、Porin OmpC 和 HSP60。I 组的 8 名患者也显示出细菌肽，而 II 组没有。与无细菌 DNA 的患者相比，所有研究的免疫激活介质在有细菌 DNA 的患者中均显著升高。与无细菌肽的患者相比，有细菌肽的患者 TNF-α、IFN-γ 和补体蛋白显著增加。在一组晚期肝硬化患者的腹水中存在细菌肽易位，并与增强的免疫反应相关。
