INTERFERON-GAMMA LEVELS IN PERITONEAL-DIALYSIS EFFLUENTS - RELATION TO PERITONITIS

Citation
Mk. Dasgupta et al., INTERFERON-GAMMA LEVELS IN PERITONEAL-DIALYSIS EFFLUENTS - RELATION TO PERITONITIS, Kidney international, 46(2), 1994, pp. 475-481
Citations number
29
Categorie Soggetti
Urology & Nephrology
Journal title
ISSN journal
00852538
Volume
46
Issue
2
Year of publication
1994
Pages
475 - 481
Database
ISI
SICI code
0085-2538(1994)46:2<475:ILIPE->2.0.ZU;2-Q
Abstract
Interferon-gamma levels in peritoneal dialysis effluents: Relation to peritonitis. As peritoneal macrophages require Interferon-gamma (IFN-g amma) for bacterial lysis, IFN-gamma levels were measured in peritonea l dialysis effluents (PDE) by a specific radioimmunoassay. High IFN-ga mma levels were found in patients with peritonitis compared to low lev els in patients without peritonitis (($) over bar x 9.73 +/- 2.63 SE U /ml, N = 39 vs. 0.25 +/- 0.04, N = 32). IFN-gamma levels varied among different bacteria: Staph. aureus (highest: 23.4 +/- 5.7, N = 14), Sta ph. epidermidis (lower: 3.2 +/- 0.8, N = 13), other gram-positive (1.0 6 +/- 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-gamma levels in 10 peritoneal dialysis patients (5 with peritonitis, 5 without), levels were raised only in PDE of patients with peritonitis, implying local IFN-gamma pr oduction. Total lymphocytes, T, B and monocyte subsets in patients' pl asma and PDE did not differ, except for a higher number of mononuclear cells in PDE of patients with peritonitis (P < 0.05). Further investi gation of in vitro IFN-gamma production in PDE with peritoneal monocyt es, syngeneic host lymphocytes, and bacteria showed that Staph. aureus induced the highest levels of IFN-gamma and E. coli the lowest, in ex periments with T cell enriched host lymphocytic fractions. We conclude that Staph. aureus peritonitis induces high levels of IFN-gamma in PD E, possibly by a T cell dependent superantigen response.