Trypanosoma congolense Infections: Induced Nitric Oxide Inhibits Parasite Growth In Vivo.

Wild-type (WT) C57BL/6 mice infected intraperitoneally with 5 × 10(6) Trypanosoma congolense survive for more than 30 days. C57BL/6 mice deficient in inducible nitric oxide synthase (iNOS(-/-)) and infected with 10(3) or 5 × 10(6) parasites do not control the parasitemia and survive for only 14 ± 7 or 6.8 ± 0.

Intradermal infections of mice by low numbers of african trypanosomes are controlled by innate resistance but enhance susceptibility to reinfection.

Antibodies are required to control blood-stage forms of African trypanosomes in humans and animals. Here, we report that intradermal infections by low numbers of African trypanosomes are controlled by innate resistance but prime the adaptive immune response to increase susceptibility to a subsequent challenge. Mice were found 100 times more resistant to intradermal infections by Trypanosoma congolense or Trypanosoma brucei than to intraperitoneal infections.

Serum biochemistry, serology, and parasitology of boreal caribou (Rangifer tarandus caribou) in the Northwest Territories, Canada.

Boreal caribou (Rangifer tarandus caribou) are an ecologically and culturally important wildlife species and now range almost exclusively in the boreal forests of Canada, including the Northwest Territories, northern Alberta, and British Columbia. Boreal caribou are threatened throughout their Canadian range because of direct and indirect natural and anthropogenic factors. In the Northwest Territories, however, they have a continuous range that overall has not yet been subjected to the same degree of anthropogenic habitat fragmentation and degradation that has occurred elsewhere in Canada.

Characterization of major surface protease homologues of Trypanosoma congolense.

Trypanosomes encode a family of proteins known as Major Surface Metalloproteases (MSPs). We have identified six putative MSPs encoded within the partially sequenced T. congolense genome.

T cells and immunopathogenesis of experimental African trypanosomiasis.

African trypanosomes are pathogens for humans and livestock. They are single-cell, extra-cellular parasites that cause persistent infections of the blood and induce profound immunosuppression. Here, we review recent work on experimental African trypanosomiasis, especially infections with Trypanosoma congolense, in mice with regard to mechanisms of immunosuppression and immunopathology.

Regulatory T cells prevent control of experimental African trypanosomiasis.

African trypanosomes are single-cell, extra-cellular blood parasites causing profound immunosuppression. Susceptible BALB/c mice infected s.c.

CR3 (CD11b/CD18) is the major macrophage receptor for IgM antibody-mediated phagocytosis of African trypanosomes: diverse effect on subsequent synthesis of tumor necrosis factor alpha and nitric oxide.

Immunoglobulin M (IgM) antibodies to the variant surface glycoproteins (VSG) of African trypanosomes are the first and predominant class of anti-trypanosomal antibodies in the infected host. They are a major factor in controlling waves of parasitemia, but not in long-term survival. The macrophage receptor(s) that enables phagocytosis of IgM anti-VSG-coated African trypanosomes is unknown.

Experimental African trypanosomiasis: a subset of pathogenic, IFN-gamma-producing, MHC class II-restricted CD4+ T cells mediates early mortality in highly susceptible mice.

Infections of highly susceptible BALB/c mice with virulent strains of Trypanosoma congolense or Trypanosoma brucei result in rapid death (8 days). We have previously shown that this mortality is IFN-gamma dependent. In this study we show that IFN-gamma is produced predominantly by CD3+Thy1.

Impaired Kupffer cells in highly susceptible mice infected with Trypanosoma congolense.

In highly susceptible BALB/c mice infected with Trypanosoma congolense, the total number of Kupffer cells in the liver remains constant; however, their mean size increases fivefold towards the terminal stage. About 25% of Kupffer cells undergo apoptosis. We suggest that development of an impairment of the macrophage system might be a major mechanism for inefficient elimination of trypanosomes.

Trypanosoma congolense infections: antibody-mediated phagocytosis by Kupffer cells.

Immunohistochemical double-label technique was used to detect trypanosomal antigen in macrophages. Immunoglobulin (Ig)M as well as IgG2a monoclonal antibodies (mAb) specific for the variant surface glycoprotein (VSG) mediated phagocytosis of Trypanosoma congolense variant antigenic type (VAT) TC13 by macrophages [bone marrow-derived macrophage cell line from BALB/c (BALB.BM)] in vitro.

Experimental African trypanosomiasis: IFN-gamma mediates early mortality.

In this study, we demonstrate that Kupffer cells in the livers of highly susceptible BALB/c mice infected with Trypanosoma congolense were loaded with trypanosomal antigen and appeared highly activated. This was associated with an enlarged capillary bed in the livers and decreased blood pressure of these mice towards the terminal stage. Blocking of murine IL-10 receptor (IL-10R)in vivo shortened the survival time of highly susceptible T.