Control of Trypanosoma evansi infection is IgM mediated and does not require a type I inflammatory response.

TitleControl of Trypanosoma evansi infection is IgM mediated and does not require a type I inflammatory response.
Publication TypeJournal Article
Year of Publication2007
AuthorsBaral, T. Nath, P. De Baetselier, F. Brombacher, and S. Magez
JournalJ Infect Dis
Volume195
Issue10
Pagination1513-20
Date Published2007 May 15
Type of Articleparasites
ISSN0022-1899
KeywordsAnimals, Cell Culture Techniques, Cytokines, Disease Models, Animal, Female, Immunoglobulin M, Inflammation, Mice, Mice, Inbred C57BL, Parasitemia, Time Factors, Trypanosoma, Trypanosomiasis, Tumor Necrosis Factor-alpha
Abstract

Very recent reports have documented that Trypanosoma evansi, the etiological agent of the livestock disease "surra," can cause human trypanosomiasis. In contrast to trypanosomes causing human African trypanosomiasis, T. evansi has a wide geographic distribution and host range, yet information about the immunobiological aspects of T. evansi trypanosomiasis is limited. Here, we show that, although T. evansi causes the induction of tumor necrosis factor (TNF), interferon-gamma, and nitric oxide during the early stage of infection, none of these molecules are crucial for parasitemia control and survival of the infected animal. However, TNF and TNF receptor 2 affect the induction of late-stage anemia. Using B cell- and immunoglobulin M (IgM)-deficient mice, we identified IgM as being crucial for parasitemia control and host survival. Collectively, our results show that, compared with other trypanosomes, T. evansi displays a distinct host-parasite interaction profile, give that, despite an infection-associated induction of proinflammatory molecules, only IgM antibodies contribute significantly to parasite control.

DOI10.1086/515577
Alternate JournalJ. Infect. Dis.
PubMed ID17436232