Abstract
Specific serum and intestinal immunoglobulin (Ig)G1 and IgA responses to Heligmosomoides polygyrus were measured in a panel of seven inbred mouse strains which exhibit 'rapid' (<6 weeks (SWRxSJL)F1), 'fast' (<8 weeks, SJL and SWR), 'intermediate' (10-20 weeks, NIH and BALB/c) or 'slow' (>25 weeks, C57BL/10 and CBA) resolution of primary infections. Mice with 'rapid', 'fast' or 'intermediate' response phenotypes produced greater serum and intestinal antibody responses than those with 'slow' phenotypes. The F1 hybrids ((SWRxSJL)F1) of two 'fast' responder strains showed the earliest antibody response with maximum titres evident within 6 weeks of infection. There was a negative correlation between the serum IgG1 responses and worm burdens in individual mice within a number of mouse strains, and also between serum IgG1 and IgA responses and worm burdens in the 'rapid' ((SWRxSJL)F1) responder strain. The presence of IgG1 in the gut was found to be due to local secretion rather than plasma leakage. Using Western immunoblotting, serum IgG1 from 'rapid' and 'fast' responder but not 'slow' responder mice was found to react with low molecular weight antigens (16-18 kDa) in adult worm excretory/secretory products.
Highlights
The trichostrongyloid nematode Heligmosomoides polygyrus, a parasite of the small intestine of the mouse, has been used extensively as an experimental model for studying host–parasite interactions during chronic infections.Marked strain-dependent variations in the kinetics of worm expulsion have been observed in both primary and secondary infections (Behnke & Robinson 1985, Enriquez et al 1988, Robinson et al 1989, Wahid et al 1989)
In an earlier paper we reported a negative correlation between the intensity of the serum adult worm-specific IgG1 antibody response and worm burden across a number of inbred mouse strains experiencing primary infection, suggesting that those strains which mounted rapid and intense IgG1 responses lost worms quickly (Wahid & Behnke 1993)
We were unable to detect any significant negative correlation between serum parasite-specific IgG1 and worm burdens within strains, as would have been expected if parasite-specific IgG1 had had a protective role during primary infections. Following on from this earlier study, we examined the relationship between host response phenotype and intestinal parasite-specific antibody activity to test the hypothesis that if antibody plays a significant role in curtailing primary infections in mice, the rapidity and intensity of the local mucosal parasite-specific antibody might be a better measure of the response phenotype than the accompanying serum response
Summary
The trichostrongyloid nematode Heligmosomoides polygyrus, a parasite of the small intestine of the mouse, has been used extensively as an experimental model for studying host–parasite interactions during chronic infections.Marked strain-dependent variations in the kinetics of worm expulsion have been observed in both primary and secondary infections (Behnke & Robinson 1985, Enriquez et al 1988, Robinson et al 1989, Wahid et al 1989). Many syngeneic strains harbour adult worms for up to 40 weeks after a primary infection, probably reflecting the natural lifespan of the parasite, whereas others curtail primary infections within 6 weeks. These strain variations are thought to reflect the influence of genetic regulation of components of the host response (Liu 1966, Behnke & Robinson 1985, Behnke 1987) and imply that in certain genotypes a successful protective immune response can be mounted during the course of a primary infection to eliminate the parasite. Not surprisingly significant correlations have been reported between the effectiveness of the secondary
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