Interferon-gamma levels in peritoneal dialysis effluents: Relation to peritonitis

Interferon-gamma levels in peritoneal dialysis effluents: Relation to peritonitis. As peritoneal macrophages require Interferon-γ (IFN-γ) for bacterial lysis, IFN-γ levels were measured in peritoneal dialysis effluents (PDE) by a specific radioimmunoassay. High IFN-γ levels were found in patients wi...

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Veröffentlicht in:Kidney international 1994-08, Vol.46 (2), p.475-481
Hauptverfasser: Dasgupta, Mrinal K., Larabie, Marlene, Halloran, Philip F.
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Sprache:eng
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Zusammenfassung:Interferon-gamma levels in peritoneal dialysis effluents: Relation to peritonitis. As peritoneal macrophages require Interferon-γ (IFN-γ) for bacterial lysis, IFN-γ levels were measured in peritoneal dialysis effluents (PDE) by a specific radioimmunoassay. High IFN-γ levels were found in patients with peritonitis compared to low levels in patients without peritonitis (x 9.73 ± 2.63 SE U/ml, N = 39 vs. 0.25 ± 0.04, N = 32). IFN-γ levels varied among different bacteria: Staph. aureus (highest: 23.4 ± 5.7, N = 14), Staph. epidermidis (lower: 3.2 ± 0.8, N = 13), other gram-positive (1.06 ± 0.32, N = 6), gram-negative bacteria (lowest: 0.57 ± 0.30, N = 6). After treatment of peritonitis levels decreased. In corresponding blood and PDE samples, by comparing IFN-γ levels in 10 peritoneal dialysis patients (5 with peritonitis, 5 without), levels were raised only in PDE of patients with peritonitis, implying local IFN-γ production. Total lymphocytes, T, B and monocyte subsets in patients' plasma and PDE did not differ, except for a higher number of mononuclear cells in PDE of patients with peritonitis (P < 0.05). Further investigation of in vitro IFN-γ production in PDE with peritoneal monocytes, syngeneic host lymphocytes, and bacteria showed that Staph. aureus induced the highest levels of IFN-γ and E. coli the lowest, in experiments with T cell enriched host lymphocytic fractions. We conclude that Staph. aureus peritonitis induces high levels of IFN-γ in PDE, possibly by a T cell dependent superantigen response.
ISSN:0085-2538
1523-1755
DOI:10.1038/ki.1994.297