Lipopolysaccharide-binding protein is present in effluents of patients with Gram-negative and Gram-positive CAPD peritonitis

BACKGROUND: Bacterial peritonitis is a frequent complication during treatment of end-stage renal failure by continuous ambulatory peritoneal dialysis. Local host defence mechanisms including the secretion of proinflammatory cytokines by peritoneal macrophages are of particular importance in the pathogenesis of infectious complications. LPS-binding protein (LBP) and soluble CD14 (sCD14) are serum factors known to regulate the endotoxin-induced cellular immune response. However, it is still unknown whether LBP and sCD14 are also present in the peritoneal effluent of CAPD patients. METHODS: Using specific immunoassays, we examined the concentration of LBP, sCD14 and the proinflammatory cytokines TNF-alpha, IL-1beta and IL-6 in the dialysis effluents of 31 patients with CAPD-associated peritonitis. Twenty patients without peritonitis served as controls. Intraperitoneal LPS concentrations were determined using the limulus amebocyte lysate assay. RESULTS: Bacterial lipopolysaccharide could be detected in 42% of the infected dialysis effluents. In comparison to controls (0.2 +/- 0.05 microg/ml), LBP was significantly elevated in both gram-negative/LPS-positive (1.03 +/- 0.3 microg/ml) and gram-positive infections (0.5 +/- 0.14 microg/ml) (P<0.05). No significant differences were detected concerning the intraperitoneal sCD14 levels in the three patient groups. Levels of TNF-alpha, IL-1beta and IL-6 were significantly increased in the effluents of patients with bacterial peritonitis compared to noninfected controls. Moreover the respective cytokine concentrations were significantly higher in the gram-negative/LPS-positive compared to the gram-positive bacterial infections (P<0.01). CONCLUSION: Our data demonstrate that LBP is significantly elevated in the dialysis effluents of patients with CAPD-associated peritonitis caused by both gram-negative and gram-positive bacteria and might be used as a marker of intraperitoneal infection. Moreover, our findings support the concept that LBP enhances the effects of LPS on cytokine production by peritoneal macrophages. The function of LBP in gram-positive infection remains to be further elucidated.