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Tumour Necrosis Factor in Hepatosplenic Schistosomiasis
Author(s) -
ZWINGENBERGER K.,
IRSCHICK E.,
SIQUEIRA J. G. VERGETTI,
DACAL A. R. CORREIA,
FELDMEIER H.
Publication year - 1990
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/j.1365-3083.1990.tb02761.x
Subject(s) - schistosomiasis , praziquantel , radioimmunoassay , tumor necrosis factor alpha , bioassay , immunology , necrosis , cytokine , medicine , biology , helminths , genetics
Periportal fibroplasia is the dominating feature of hepatosplenic schistosomiasis. Since monokines play an Important role in the regulation of fibroplasia, tumour necrosis factor (TNF) and interleukin 1β (IL‐1β) were assessed in sera and cell culture supernatants from patients with intestinal and hepatosplenic schistosomiasis before and 3‐6 months after treatment with praziquantel. Uninfected controls were from the study area in Alagoas, Brazil. TNF was measured using an L‐M mouse fibroblast bioassay and radioimmunoassays specific for TNF‐α. Whereas TNF‐α was elevated three fold in the patients' sera, three‐to five‐fold reductions of TNF were observed by radioimmunoassay and bioassay, respectively, in cell culture supernatants of hepatosplenic schistosomiasis patients. Significant deviations, in opposite directions, from TNF levels in control sera and supernatants are most plausible in the event of a sequestration of TNFα‐producing cells from the circulation. This process may be disease stage‐specific since a dichotomy between incipient and advanced cases of hepatosplenic schistosomiasis became apparent in the amplitude and kinetics of changes during the follow‐up after treatment.