PATHOGENESIS OF ONCHOCERCAL DERMATITIS - POSSIBLE ROLE OF PARASITE PROTEASES AND AUTOANTIBODIES TO EXTRACELLULAR-MATRIX PROTEINS

Citation
I. Petralanda et Wf. Piessens, PATHOGENESIS OF ONCHOCERCAL DERMATITIS - POSSIBLE ROLE OF PARASITE PROTEASES AND AUTOANTIBODIES TO EXTRACELLULAR-MATRIX PROTEINS, Experimental parasitology, 79(2), 1994, pp. 177-186
Citations number
47
Categorie Soggetti
Parasitiology
Journal title
ISSN journal
00144894
Volume
79
Issue
2
Year of publication
1994
Pages
177 - 186
Database
ISI
SICI code
0014-4894(1994)79:2<177:POOD-P>2.0.ZU;2-R
Abstract
We examined the immunogenicity of various connective tissue proteins i n patients with chronic onchocercal dermatitis and the effect of filar ial proteases on this host-parasite interaction. Sera from patients wi th onchocerciasis reacted strongly with cuticular collagens from filar ial parasites and with mammalian laminin. Some sera also contained ant ibodies to elastin and collagen type IV, but none reacted with collage n types I-III or fibronectin. This pattern of reactivity was character istic for onchocerciasis: sera from patients with mansonellosis reacte d strongly with collagen type IV but only weakly with laminin. Reactiv ity with mammalian laminin or collagen could not be absorbed with cuti cular proteins from filarial worms and vice versa. Digestion fragments of laminin treated with filarial proteases retain antigenic determina nts recognized by sera from patients with onchocerciasis. In contrast, proteases from Onchocerca volvulus adults and microfilariae drastical ly decreased the reactivity of the same sera with collagen type IV. Th ese results indicate that filarial proteases may contribute to the pat hogenesis of chronic onchocercal dermatitis, directly, by enzymaticall y destroying connective tissue of the skin, and indirectly, by trigger ing autoimmune responses to self-determinants on connective tissue pro teins that are normally hidden within the supramolecular structure of the extracellular matrix complex. (C) 1994 Academic Press, Inc.