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The influence of Heligmosomoides polygyrus on infection with Trichinella spiralis was studied in BALB/c mice. Mice coinfected with T. spiralis and previously given H. Polygyrus harboured both nematode species till day 34. The number of T. spiralis muscle larvae was greater in mice coinfected with H. polygyrus/T. spiralis or T. spiralis/H. polygyrus than after infection with T. spiralis alone. Infection with H. polygyrus did not enhance eosinophil and IL-5 levels induced by T. spiralis. Additionally, the production of IgG1 specific to LI T. spiralis was inhibited by co-infection. Changes in the levels of IFN-y and IgG2a implicated a disturbance in Th2 cell activation during protective response and resulted in the greater number of T. spiralis muscle larvae in coinfected mice.
The aim of this study was to examine whether the profile of IgG1 and IgG2a responses to Trichinella spiralis is changed by subsequent infection with Heligmosomoides polygyrus. IgG1 and IgG2a antibodies were analysed in terms of Th2 related events evoked by both species of nematodes, although with a different parasitic result. T. spiralis antigens were recognized by IgG1 antibody from mice infected with T. spiralis and/or with H. polygyrus. IgG1 antibody from mice infected with T. spiralis did not recognize excretory-secretory H. polygyrus products. IgG2a antibodies from a T. spiralis and/or H. polygyrus infection recognized somatic antigens of H. polygyrus. T. spiralis antigens were only specifically recognized by IgG2a from T. spiralis infected mice. Subsequent infection with H. polygyrus inhibited the recognition of T. spiralis antigens. Previous infection with T. spiralis had only marginal effects on the course of H. polygyrus infection. Additionally, H. polygyrus altered the IgG1 and IgG2a profile of antibody responses to T. spiralis.
GI nematodes are most commonly controlled by chemotherapy. Anthelmintic efficacy is decreasing as drug resistance becomes widespread and other approaches are needed. Knowledge of protective immunity against GI parasites is important for the development of vaccine strategies. Success in this field is presently limited, and parasites have many ways of evading immunity. An alternative approach is selection and breeding of genetically resistant stock. This requires definition of the genes responsible and identification of markers for selection. It is well known that resistance to infection is variable within host species but little progress has been made in defining the genes responsible. We describe an approach to identifying the genes responsible for resistance of mice to Heligmosomoides polygyrus as a model for identification of homologous genes in domestic animals. F2 and eventually F6 generations from crosses between resistant SWR and susceptible CBA strains are being phenotyped for parasitological and immunological traits. Microsatellite mapping will then identify the chromosomal locations and eventually the specific loci concerned. Data from this project will facilitate breeding programmes and lead to a greater understanding of the roles of specific genes and their products in particular resistance mechanisms.
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