Hostname: page-component-586b7cd67f-dsjbd Total loading time: 0 Render date: 2024-11-28T03:34:45.537Z Has data issue: false hasContentIssue false

Variation in responsiveness to Trichinella spiralis infection in inbred rat strains

Published online by Cambridge University Press:  06 April 2009

R. G. Bell
Affiliation:
James A. Baker Institute for Animal Health, NYS College of Veterinary Medicine, Cornell University, Ithaca, NY 14853

Extract

An analysis of interstrain variation between 12 inbred and 4 congenic rat strains in the expression of immunity against Trichinella spiralis is reported. All rat strains expressed strong rapid expulsion which resulted in the elimination of 88–98% of a challenge infection of muscle larvae. In contrast, substantial interstrain variation in the rate of adult worm expulsion in the primary infection as evident. By day 10 after infection, BUF and YO strains had < 50 worms left in the intestine whereas BI and WKA strain rats had barely begun rejection, with approximately 1000 worms present in the gut for both strains. All other rat strains fell within these extremes in a continuous gradation. There was no clustering of rat strains into phenotypic groups with comparable worm burdens as seen with mice. The number of muscle larvae that established after the primary infection showed less variation than had adult worm burden in the primary infection and there was only a weak correlation of muscle larvae burden with numbers of intestinal adults present at 10 days. Comparison of MHC matched or MHC-disparate rat strains on a PVG background suggested that non-MHC genes determined the principal adult worm rejection characteristics of a given strain. The absence of phenotypic variation in the expression of rapid expulsion in rats reinforces the biological distinction between rat rapid expulsion and the ‘rapid expulsion’ defined for mice

Type
Research Article
Copyright
Copyright © Cambridge University Press 1992

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

References

REFERENCES

Altman, P. L. & Katz, D. D.Inbred and Genetically Defined Strains of Laboratory Animals. Part 1. Mouse and Rat. Bethesda, MD: Federation of American Societies for Experimental Biology.Google Scholar
Bell, R. G. (1988). Genetic analysis of expulsion of adult Trichinella spiralis in NFS, C3H/He, and B10.BR mice. Experimental Parasitology 66, 5765.CrossRefGoogle ScholarPubMed
Bell, R. G. (1992). Trichinella spiralis: Evidence that mice do not express rapid expulsion. Experimental Parasitology 14 (in the Press).Google Scholar
Bell, R. G. & Liu, W.-M. (1988). Trichinella spiralis: quantitative relationship between intestinal worm burden, worm rejection, and the measurement of intestinal immunity in inbred mice. Experimental Parasitology 66, 4456.CrossRefGoogle ScholarPubMed
Bell, R. G., Mcgregor, D. D. & Adams, L. S. (1982 a). Trichinella spiralis: characterization and strain distribution of rapid expulsion in inbred mice. Experimental Parasitology 53, 301–14.CrossRefGoogle ScholarPubMed
Bell, R. G., Mcgregor, D. D. & Adams, L. S. (1982 b). Trichinella spiralis: genetic basis for differential expression of phase-specific intestinal immunity in inbred mice. Experimental Parasitology 53, 315–25.CrossRefGoogle ScholarPubMed
Bell, R. G., Mcgregor, D. D. & Despommier, D. D. (1979). Trichinella spiralis: mediation of the intestinal component of protective immunity in the rat by multiple, phase-specific antiparasitic responses. Experimental Parasitology 47, 140–57.CrossRefGoogle ScholarPubMed
Bell, R. G., Wang, C. H. & Ogden, R. W. (1985). Trichinella spiralis: nonspecific resistance and immunity to newborn larvae in inbred mice. Experimental Parasitology 60, 101–10.Google ScholarPubMed
Crocker, P. R., Blackwell, J. M., Bradley, D. J. (1984). Expression of natural resistance gene Lsh in resident liver macrophages. Infection and Immunity 43, 434–9.CrossRefGoogle ScholarPubMed
Cruikshank, J. K., Price, K. M., Mackenzie, C. D., Spry, C. J. F. & Denham, D. A. (1983). Infection of inbred and nude (athymic) rats with Brugia spp. Parasite Immunology 5, 527–37.CrossRefGoogle Scholar
Detolla, L. J. Jr., Scott, P. A. & Farrell, J. P. (1981). Single gene control of resistance to cutaneous leishmaniasis in mice. Immunogenetics 14, 2939.CrossRefGoogle ScholarPubMed
Fox, E. G. & Schacher, J. F. (1976). A comparison of syngeneic laboratory rat-strains as hosts for Brugia pahangi. Transactions of the Royal Society of Tropical Medicine and Hygiene 70, 523.CrossRefGoogle ScholarPubMed
Gill, T. J. III, Kunz, M. W., Misra, D. N. & Hassett, A. L. C. (1987). The major histocompatibility complex of the rat. Transplantation 43, 773–85.CrossRefGoogle ScholarPubMed
Good, M. F., Berzofsky, J. A., Maloy, W. L., Mayashi, Y., Fuji, N., Hockmeyer, W. T. & Miller, L. H. (1986). Genetic control of the immune response in mice to a Plasmodium falciparum sporozoite vaccine. Widespread nonresponsiveness to a single malaria T epitope in highly repetitive vaccine. Journal of Experimental Medicine 164, 655–60.CrossRefGoogle ScholarPubMed
Hill, A. V. S. (1987). Haemoglobinopathies and malaria: new approaches to an old hypothesis. Parasitology Today 3, 83–5.CrossRefGoogle Scholar
Hormaeche, C. (1979). Genetics of natural resistance to salmonellae in mice. Immunology 37, 318–27.Google ScholarPubMed
Khamboonruang, C. (1971). Output of larvae and life span of Trichinella spiralis in relation to worm burden superinfection in the mouse. Journal of Parasitology 57, 289–97.CrossRefGoogle ScholarPubMed
Kirkland, T. N. & Fierer, J. (1985). Genetic control of resistance to Coccidioides immitis: a single gene that is expressed in spleen cells determines resistance. Journal of Immunology 135, 548–52.CrossRefGoogle ScholarPubMed
Madden, K. B., Murrell, K. D. & Lunney, J. K. (1990). Trichinella spiralis: major histocompatibility complex-associated elimination of encysted muscle larvae in swine. Experimental Parasitology 70, 443–51.CrossRefGoogle ScholarPubMed
Mitchell, G. F. (1989). Portal system peculiarities may contribute to resistance against schistosomes in 129/J mice. Parasite Immunology 11, 713–17.CrossRefGoogle ScholarPubMed
Rousseaux-Prevost, R., Bazin, H. & Capron, A. (1977). IgE in experimental schistosomiasis. 1. Serum IgE levels after infection by Schistosoma mansoni in various strains of rats. Immunology 35, 501–11.Google Scholar
Trishmann, T. M. (1986). Trypanosoma cruzi: early parasite proliferation and host resistance in inbred strains of mice. Experimental Parasitology 62, 194201.CrossRefGoogle Scholar
Wakelin, D. (1980). Genetic control of immunity to parasites: infection with Trichinella spiralis in inbred and congenic mice showing rapid and slow responses to infection. Parasite Immunology 2, 8598.CrossRefGoogle Scholar
Wassom, D. L., David, C. S. & Gleich, G. J. (1979). Genes within the major histocompatibility complex influence susceptibility to Trichinella spiralis in the mouse. Immunogenetics 9, 491–6.CrossRefGoogle Scholar
Wassom, D. L. & Kelly, E. A. B. (1990). The role of the major histocompatibility complex in resistance to parasite infections. Critical Reviews in Immunology 10, 3152.Google ScholarPubMed
Wassom, D. L., Wakelin, D., Brooks, B. O., Krco, C. J. & David, C. S. (1984). Genetic control of immunity to Trichinella spiralis infections in mice. Hypothesis to explain the role of H-2 genes in primary and challenge infections. Immunology 51, 625–61.Google ScholarPubMed