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The effects of tumour necrosis factor on host—parasite relations in murine Mesocestoides corti (Cestoda) infection

Published online by Cambridge University Press:  06 April 2009

P. Jenkins
Affiliation:
Departments of Veterinary Pathology, University of Liverpool, Liverpool L69 3BX
S. Spiers
Affiliation:
Departments of Veterinary Clinical Sciences, University of Liverpool, Liverpool L69 3BX
J. B. Dixon
Affiliation:
Departments of Veterinary Pathology, University of Liverpool, Liverpool L69 3BX
S. D. Carter
Affiliation:
Departments of Veterinary Pathology, University of Liverpool, Liverpool L69 3BX Departments of Veterinary Clinical Sciences, University of Liverpool, Liverpool L69 3BX
S. May
Affiliation:
Departments of Veterinary Clinical Sciences, University of Liverpool, Liverpool L69 3BX

Summary

The regulatory role of tumour necrosis factor (TNF) was investigated in murine infection with tetrathyridia of Mesocestoides corti. Recombinant TNFα reduced macrophage larvicidal activity in vitro. M. corti primed mice for TNF release in response to bacterial lipopolysaccharide (LPS) in vivo. TNF activity was amplified 100-fold at 14 days post-infection (p.i.), with a further rise at day 28 p.i. Maximal inflammatory reaction was observed histologically in the liver at the height of TNF activity. Hepatic necrosis was located within inflammatory foci, but not within the vicinity of the parasite itself, suggesting that TNF may contribute to the pathogenesis of infection. Peritoneal cells from infected mice, when stimulated with tetrathyridia in vitro, showed a 4-fold increase in TNFα activity at day 14 p.i. However, when peritoneal cells were stimulated with LPS in vitro, a marked increase in TNFα secretion was observed at 2 months post-infection followed by a slow decline. It is suggested that impaired macrophage effector function, previously attributed to endogenous endotoxin, which gains access to peritoneal macrophages through an inability of the liver to detoxify endotoxin, may be mediated through TNFα.

Type
Research Article
Copyright
Copyright © Cambridge University Press 1992

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