Different peripheral neuroendocrine responses to Trypanosoma cruzi infection in mice lacking adaptive immunity

• Published in: Annals of the New York Academy of Sciences 2012-07, Vol.1262 (1), p.37-44
• Main Authors: Roggero, Eduardo, Wildmann, Johannes, Passerini, Marcelo O., del Rey, Adriana, Besedovsky, Hugo O.
• Format: Article
• Language: English
• Subjects: Adaptive Immunity; Animals; Blood; Chagas Disease - immunology; Chagas Disease - parasitology; Chagas Disease - physiopathology; corticosterone; Corticosterone - metabolism; Cytokines - blood; Disease Models, Animal; Genes; Homeodomain Proteins - genetics; Homeodomain Proteins - immunology; Host-Parasite Interactions - immunology; Host-Parasite Interactions - physiology; Hydroxyindoleacetic Acid - metabolism; Immunity; infection; Infections; Lymph; Lymphocytes; Mice; Mice, Inbred C57BL; Mice, Knockout; Mortality; Neuroimmunomodulation; Neurosecretory Systems - immunology; Neurosecretory Systems - physiopathology; noradrenaline; Norepinephrine - metabolism; Parasites; Protozoa; recombinase activator gene 1-deficient mice; Rodents; serotonin; Serotonin - metabolism; sympathetic nervous system; Trypanosoma cruzi; Trypanosoma cruzi - immunology
• ISSN: 0077-8923; 1749-6632
• DOI: 10.1111/j.1749-6632.2012.06645.x

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.