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Neuroendocrine‐immunology of Experimental Chagas' Disease
Author(s) -
Roggero Eduardo,
Pérez Ana R.,
Bottasso Oscar A.,
Besedovsky Hugo O.,
Del Rey Adriana
Publication year - 2009
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.1749-6632.2008.03982.x
Subject(s) - immunology , endocrine system , cytokine , biology , tumor necrosis factor alpha , corticosterone , immune system , chagas disease , cd8 , endocrinology , hormone
The cytokine‐mediated stimulation of the hypothalamus–pituitary–adrenal (HPA) axis is relevant for immunoregulation and survival during bacterial endotoxemia and certain viral infections. However, only limited information is available regarding the effect of endogenous glucocorticoids on parasitic diseases. Here, we discuss evidence that the increased levels of corticosterone that occur following Trypanosoma cruzi infection in mice is an endocrine response that protects the host by impeding an excessive production of pro‐inflammatory cytokines. Comparative studies between susceptible C57Bl/6J and resistant Balb/c mice indicate that the predisposition to the disease depends on the appropriate timing and magnitude of the activation of the HPA axis. However, this endocrine response also results in thymus atrophy and depletion of CD4 + CD8 + by apoptosis. On the other hand, using tumor necrosis factor (TNF)‐receptor knockout mice, we found that TNF‐α plays a complex role during this disease; it is involved in the mediation of cardiac tissue damage but it also contributes to prolonged survival. Taken together, this evidence indicates that a subtle balance between endocrine responses and cytokine production is necessary for an efficient defense against T . cruzi infection.