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• W1970783022 abstract "Background: Peritonitis is the most serious complication of peritoneal dialysis (PD). We previously showed that high levels of interleukin (IL)-12 and IL-18 in PD effluents (PDE) during the early phase of peritonitis correlated with a predominant Type 1 immune response and a favorable outcome in PD-related peritonitis. To further clarify the longitudinal changes of peritoneal immunity during PD-related peritonitis, we examined the kinetic production of IL-17 in PDE during peritonitis. The correlation between the IL-17 expression pattern and peritonitis outcome was analyzed. Methods: The levels of IL-17 were measured in PDE during various phases of peritonitis in 38 patients undergoing PD. The patients were divided into two groups, according to whether they had a rapid versus a delayed response to antibiotic treatment. Results: The kinetic expression of IL-17, as measured by enzyme-linked immunosorbent assay, differed between the two groups. In the rapid response group, high level of IL-17 was detected in PDE initially and progressively decreased during treatment. In the delayed response group, IL-17 levels in PDE were persistently low throughout the whole course of treatment. In the early phase of peritonitis, the IL-17 levels in PDE were significantly higher in the rapid response group (p < 0.05). Conclusion: These data suggested that local IL-17 production is part of a protective early immune response to PD-related peritonitis. High levels of IL-17 in PDE during the early phase of peritonitis correlated with a favorable outcome. Manipulation of IL-17 cytokine expression in patients with peritonitis may modulate peritoneal immune response and affect peritonitis outcome." @default.
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• W1970783022 date "2011-01-01" @default.
• W1970783022 modified "2023-10-18" @default.
• W1970783022 title "Kinetics and involvement of interleukin-17 in the outcome of peritonitis in nondiabetic patients undergoing peritoneal dialysis☆" @default.
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• W1970783022 doi "https://doi.org/10.1016/j.jcma.2011.01.002" @default.
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