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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 ,
S. Spiers ,
J. B. Dixon ,
S. D. Carter  and
S. May
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
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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.

Keywords

Mesocestoides cortiTNFαmacrophageeffectorLPSsusceptibility
Type
Research Article
Information
Parasitology , Volume 105 , Issue 3 , December 1992 , pp. 453 - 459
Copyright
Copyright © Cambridge University Press 1992

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References

REFERENCES

Aggarwal, B. B., Aiyer, R. A., Pennica, D., Gray, P. W. & Goeddel, D. V. (1987). Human tumour necrosis factors: structure and receptor interactions. In Tumour Necrosis Factor and Related Cytotoxins. Ciba Foundation Symposium 131, pp. 39–51. Chichester: Wiley.Google Scholar
Bachwich, P. R., Chensue, S. W., Larrick, J. W. & Kunkel, S. L. (1986). Tumour necrosis factor stimulates interleukin 1 and prostaglandin E2 production in resting macrophages. Biochemical and Biophysical Research Communications 136, 94–101.CrossRefGoogle ScholarPubMed
Beutler, B. & Cerami, A. (1986). Cachectin and tumor necrosis factor as two sides of the same biological coin. Nature, London 320, 580–8.CrossRefGoogle ScholarPubMed
Beutler, B. A., Milsark, I. W. & Cerami, A. (1985). Cachectin, tumor necrosis factor: production, distribution and metabolic function in vitro. Journal of Immunology 135, 3972–9.CrossRefGoogle Scholar
Clark, I. A. & Chaudhri, G. (1988). Roles of tumor necrosis factor in malaria. In Tumor Necrosis Factor/Cachectin and Related Cytokines (ed. Bonavida, B., Gifford, G. E., Kirchner, H. & Old, L. J.), pp. 340–5. Basel: Karger.Google Scholar
Durum, S. K. & Oppenheim, J. J. (1989). Macrophagederived mediators: Interleukin 1, tumor necrosis factor, interleukin 6, interferon and related cytokines. In Fundamental Immunology (ed. Paul, W. E.), pp. 639–61. New York: Raven Press.Google Scholar
Esparza, I., Mannel, D., Ruppel, A., Falk, W. & Krammer, P. H. (1987). Interferon-γ and lymphotoxin or tumor necrosis factor act synergistically to induce macrophage killing of tumor cells and schistosomula of Schistosoma mansoni. Journal of Experimental Medicine 166, 589–95.CrossRefGoogle ScholarPubMed
Flick, D. A. & Gifford, C. E. (1984). Comparison of in vitro cell cytotoxic assays for tumor necrosis factor. Journal of Immunological Methods 68, 167–75.CrossRefGoogle ScholarPubMed
James, S. L., Glaven, J., Goldenberg, S., Meltzer, M. S. & Pearce, E. (1990). Tumour necrosis factor (TNF) as a mediator of macrophage helminthotoxic activity. Parasite Immunology 12, 1–13.CrossRefGoogle ScholarPubMed
Jenkins, P., Dixon, J. B., Rakha, N. K. & Carter, S. D. (1990). Regulation of macrophage-mediated larvicidal activity in Echinococcus granulosus and Mesocestoides corti (Cestoda) infection in mice. Parasitology 100, 309–15.CrossRefGoogle ScholarPubMed
Jenkins, P., Dixon, J. B., Haywood, S., Rakha, N. K. & Carter, S. D. (1991). Differential regulation of murine Mesocestoides corti infection by bacterial lipopolysaccharide and interferon-γ. Parasitology 102, 125–32.CrossRefGoogle ScholarPubMed
Mitchell, G. F. & Handman, E. (1977). Studies on immune responses to larval cestodes in mice: a simple mechanism of non-specific immunosuppression in Mesocestoides corti-infected mice. Australian Journal of Experimental Biology and Medical Science 55, 615–22.CrossRefGoogle ScholarPubMed
Mosmann, T. (1983). Rapid colorimetric assay for cellular growth and survival: application to proliferation and cytotoxic assays. Journal of Immunological Methods 65, 55–63.CrossRefGoogle Scholar
Old, L. J. (1985). Tumor necrosis factor (TNF). Science 230, 630–2.CrossRefGoogle ScholarPubMed
Rakha, N. K., Dixon, J. B., Skerritt, G. C., Carter, S. D., Jenkins, P. & Marshall-Clarke, S. (1991 a). Lymphoreticular responses to metacestodes: Taenia multiceps (Cestoda) can modify interaction between accessory cells and responder cells during lymphocyte activation. Parasitology 102, 133–40.CrossRefGoogle ScholarPubMed
Rakha, N. K., Dixon, J. B., Carter, S. D., Craig, P. S., Jenkins, P. & Folkard, S. (1991 b). Echinococcus multilocularis antigens modify accessory cell function in macrophages. Immunology 74, 652–6.Google Scholar
Titus, R. G., Sherry, B. & Cerami, A. (1991). The involvement of TNF, IL-1 and IL-6 in the immune response to protozoan parasites. In Immunoparasitology Today, (ed. Ash, C. & Gallagher, R. B.), pp. A13–A16. Cambridge: Elsevier Trends Journals.Google Scholar
Tracey, K. J., Lowry, S. F. & Cerami, A. (1987). Physiological responses to cachectin. In Tumour Necrosis Factor and Related Cytotoxins. Ciba Foundation Symposium 131, pp. 88–108. Chichester: Wiley.Google Scholar
Watanabe, Y. & Jacob, C. O. (1991). Regulation of MHC class II antigen expression. Opposing effects of tumor necrosis factor-α on IFN-γ-induced HLA-DR and Ia expression depends on the maturation and differentiation stage of the cell. Journal of Immunology 146, 899–905.CrossRefGoogle ScholarPubMed
Zuckerman, S. H., Evans, G. F., Snyder, Y. M. & Roeder, W. D. (1989). Endotoxin-macrophage interaction: posttranslational regulation of tumor necrosis factor expression. Journal of Immunology 143, 1223–7.CrossRefGoogle ScholarPubMed