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An immunohistological study of phenotypic characteristics of cells of the inflammatory response in the intestine of Schistosoma bovis-infected goats

Published online by Cambridge University Press:  01 January 1999

R. LINDBERG
Affiliation:
Department of Pathology, Faculty of Veterinary Medicine, Swedish University of Agricultural Sciences, P.O. Box 7028, S-75007 Uppsala, Sweden
M. V. JOHANSEN
Affiliation:
Danish Bilharziasis Laboratory, Jaegersborg Allé 1 D, DK-2920 Charlottenlund, Denmark
C. NILSSON
Affiliation:
Department of Pathology, Faculty of Veterinary Medicine, Swedish University of Agricultural Sciences, P.O. Box 7028, S-75007 Uppsala, Sweden
P. NANSEN
Affiliation:
Danish Centre for Experimental Parasitology, The Royal Veterinary and Agricultural University, Bülowsvej 13, DK-1870 Frederiksberg C, Denmark
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Abstract

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The cellular inflammatory response in the small intestine of 21 goats infected with Schistosoma bovis was phenotypically characterized by immunohistochemistry between 6 and 32 weeks post-exposure, with particular reference to perioval granulomatous reactions. Macrophages of granulomas consistently expressed MHC class II molecules, whereas multi-nucleated giant cells in general did not. Most granulomas contained moderate infiltrates of CD2+ (CD4+ or CD8+) and γ/δ (T19+) T cells, whereas B lymphocytes were sparse. Intact extravascular mucosal eggs, lacking appreciable cellular reactivity on plain histopathology, displayed surrounding collars of MHC class II+ macrophages. Gamma/delta T cells and MHC class II+ macrophages were the predominant cell types in perivascular inflammatory cell clusters in the submucosa. The phenotypic cellular composition of granulomas did not change appreciably with duration of infection. The results indicate the importance of MHC class II-restricted immune events in the caprine S. bovis egg granulomas and also suggest a role of γ/δ T cells in their pathogenesis. It is hypothesized that the early appearance of perioval macrophage collars may serve to protect eggs from ovicidal host defence mechanisms, facilitating excretion and continuation of the life-cycle.

Type
Research Article
Copyright
1999 Cambridge University Press