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Different peripheral neuroendocrine responses to Trypanosoma cruzi infection in mice lacking adaptive immunity
Author(s) -
Roggero Eduardo,
Wildmann Johannes,
Passerini Marcelo O.,
del Rey Adriana,
Besedovsky Hugo O.
Publication year - 2012
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.2012.06645.x
Subject(s) - parasitemia , biology , trypanosoma cruzi , immunity , acquired immune system , chagas disease , spleen , immunology , immune system , lymph , endocrinology , medicine , parasite hosting , malaria , pathology , plasmodium falciparum , world wide web , computer science
Trypanosoma cruzi infection in mice triggers neuroendocrine responses that affect the course of the disease. To analyze the contribution of adaptive immunity to these responses, comparative studies between normal C57Bl/6J and recombinase activator gene 1 (RAG‐1)–deficient mice, which lack mature B and T lymphocytes, were performed. There was no difference between both types of mice in basal body weight. Following infection, higher parasitemia, increased IL‐1β and IL‐6 blood levels, less marked changes in lymphoid organs weight, no cardiomegaly, and earlier mortality were observed in RAG‐1–deficient, compared with normal mice. The response of the hypothalamus–pituitary–adrenal axis after infection occurred earlier and was more intense in RAG‐1–deficient mice than in normal mice. Noradrenaline concentration and serotonergic metabolism in the spleen, lymph nodes, and heart differed between RAG‐1–deficient and normal mice. Our studies indicate that the absence of adaptive immunity to T. cruzi influences the neuroendocrine response to the infection with this parasite.