Genetics of murine resistance to Trypanosoma cruzi

Trischmann, Thomas M.; Bloom, Barry R.

doi:10.1128/iai.35.2.546-551.1982

Cited by 77 publications

(26 citation statements)

References 20 publications

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“…Several models of T. cruzi infection exist, employing various strains of mice and parasites, and these exhibit differences in parasite tropism of cells and development of disease, particularly in relation to host sex and age [28,29]. We detected the highest tissue parasite burden in the spleen.…”

Section: Discussionmentioning

confidence: 71%

Cytokine Production in Hearts of Trypanosoma cruzi‐Infected CBA Mice: Do Cytokine Patterns in Chronic Stage Reflect the Establishment of Myocardial Pathology?

et al. 1996

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The authors analysed cytokine production in hearts of Trypanosoma cruzi-infected CBA-J mice by in situ immunocytochemical staining. Cellular infiltrates were recorded in hearts from both acute and chronic stages, but were not apparent in control hearts. In the acute heart, CD8 cells predominated, with associated production of IL-4, IL-6 and TNF-alpha. Cytokine production was characterized by IL-4, IL-5, IL-6 and TNF-alpha in the chronic heart, and numbers of CD4 and CD8 cells were more equal. At this stage, calcified infarctions and associated fibrosis were apparent, mimicking chronic human Chagas' heart pathology. The authors consider the CBA mouse an appropriate model of chronic T. cruzi infection, and suggest that local cytokine production reflects establishment of heart pathology.

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Section: Discussionmentioning

confidence: 71%

Cytokine Production in Hearts of Trypanosoma cruzi‐Infected CBA Mice: Do Cytokine Patterns in Chronic Stage Reflect the Establishment of Myocardial Pathology?

et al. 1996

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“…Murine studies have demonstrated that host genetics may influence resistance to acute infection. Yet, only a few studies haveexamined the role of host genes in regulating survival, and among these studies conflicting results have been reported (Trischmann et al 1978, Trischmann & Bloom 1982, Wrightsman, Krassner & Watson 1982, Trischmann 1983, Wrightsman et al 1984, Juri, Ferreira, Ramos & Hoecker, 1990.…”

Section: Introductionmentioning

confidence: 99%

Host genetics and resistance to acute Trypanosoma cruzi infection in mice. I. Antibody isotype profiles

Powell

Wassom

1993

Parasite Immunology

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Some strains of inbred mice survive acute infection with Trypanosoma cruzi while others die within a few weeks after infection. Mice which express B10 background genes and either the H-2q or H-2d haplotypes are resistant and survive. However, mice which share the B10 genetic background but express H-2k alleles die, usually within 4 weeks following infection. These data confirm that at least 1 gene in the major histocompatibility complex can determine whether an animal lives or dies during the acute phase. Expression of the H-2q haplotype on the B10 genetic background or in DBA/1 mice is associated with resistance, but H-2q mice expressing the C3H background are susceptible. Therefore, at least 1 gene in the genetic background also influences resistance. Our data suggest that genes associated with resistance must be present in both the MHC and the genetic background or the animal will die. The isotypes and specificities of parasite reactive antibodies found in the serum of different inbred mouse strains were assessed during acute infection. Levels of IgM were higher in sera from mice which express the resistant B10 background than in sera from mice expressing the susceptible C3H background. Conversely, mice which share the C3H background genes produced high levels of anti-parasite IgG2a when compared to B10 congenic strains. Antigen specificity, however, may be influenced by both background and MHC genes, as congenic strains expressing different MHC haplotypes recognized different constellations of T. cruzi antigens.(ABSTRACT TRUNCATED AT 250 WORDS)

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“…Infection may also lead to acute disease with fatal outcome or, more commonly, the development of chronic disease with severe associated pathologies. In mice, different inbred strains may develop fatal or very mild infections when inoculated with the same T. cruzi isolate (1,2). Similarly, different T. cruzi isolates produce variable courses of infection within a given mouse strain (3).…”

mentioning

confidence: 99%

Interleukin 10 and interferon gamma regulation of experimental Trypanosoma cruzi infection.

Silva

Morrissey

Grabstein

et al. 1992

The Journal of Experimental Medicine

346

224

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SummaryStudies were undertaken to determine whether interleukin 10, (Ibl0) a cytokine shown to inhibit interferon 3' (IFN-~/) production, was involved in Tryfanosoma cruzi infections in mice. Exogenous IFN-3, protects mice from fatal infection with T. ctuzi. Furthermore, resistant B6D2 mice developed fatal T. cruzi infections when treated with neutralizing anti-IFN-3, monoclonal antibody (mAb). Thus, endogenous as well as exogenous IFN-3' is important in mediating resistance to this parasite. Because both T. cruzi-susceptible (B6) and -resistant (B6D2) mouse strains produced IFN-3, during acute infection, we looked for the concomitant production of mediators that could interfere with IFN-3,-mediated resistance to T. cruzi. We found that IL-10-specific mRNA was produced in the spleens of mice with acute T. cruzi infections. In addition, spleen cell culture supernatants from infected B6 mice, and to a lesser extent B6D2 mice, elaborated an inhibitor(s) of IFN-3' production. This inhibitor(s) was neutralized by anti-Ibl0 mAb. These experiments demonstrated the production of biologically active IL-10 during T. cruzi infection. In further studies in vitro, it was shown that IL-10 blocked the ability of IFN-'y to inhibit the intraceUular replication of T. cruzi in mouse peritoneal macrophages. Thus, in addition to its known ability to inhibit the production of IFN-% Ibl0 (cytokine synthesis inhibitory factor), may also inhibit the effects of IFN-% These experiments demonstrate that IL-10 is produced during infection with a protozoan parasite and suggest a regulatory role for this cytokine in the mediation of susceptibility to acute disease.

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Genetics of murine resistance to Trypanosoma cruzi

Cited by 77 publications

References 20 publications

Cytokine Production in Hearts of Trypanosoma cruzi‐Infected CBA Mice: Do Cytokine Patterns in Chronic Stage Reflect the Establishment of Myocardial Pathology?

Cytokine Production in Hearts of Trypanosoma cruzi‐Infected CBA Mice: Do Cytokine Patterns in Chronic Stage Reflect the Establishment of Myocardial Pathology?

Host genetics and resistance to acute Trypanosoma cruzi infection in mice. I. Antibody isotype profiles

Interleukin 10 and interferon gamma regulation of experimental Trypanosoma cruzi infection.

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