HOME HELP CONTACT US SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via ISI Web of Science (5) Citing Articles via Google Scholar Google Scholar Articles by Roggero, E. Articles by del Rey, A. Search for Related Content PubMed PubMed Citation Articles by Roggero, E. Articles by del Rey, A.

Instituto de Inmunología, Facultad de Ciencias Médicas, Santa Fé 3100, Universidad Nacional de Rosario, 2000 Rosario, Argentina
¹ Ilex-Conicet, Instituto de Investigaciones Hematológicas, Pacheco de Melo 308, Academia Nacional de Medicina, 1425 Buenos Aires, Argentina
² Department of Immunophysiology, Institute of Physiology, Medical Faculty, Deutschhausstrasse 2, Philipps University, 35037 Marburg, Germany

(Requests for offprints should be addressed to A del Rey; Email: delrey{at}mailer.uni-marburg.de)

The cytokine-mediated stimulation of the hypothalamus–pituitary–adrenal (HPA) axis is relevant for survival during bacterial endotoxemia and certain viral infections. However, only limited information is available regarding the effects of endogenous glucocorticoids on parasite diseases. We have studied this issue using, as a model, C57Bl/6 and Balb/c mice infected with Trypanosoma cruzi, the causal agent of Chagas’ disease. These two mouse strains differ in the susceptibility to infection with the parasite. An intense stimulation of the HPA-axis was observed 3 weeks after infection in both strains, but glucocorticoid levels were already increased two- to threefold in the less susceptible Balb/c strain during the first week. Blockade of glucocorticoid receptors with the glucocorticoid antagonist RU486, starting on day 10 after infection, partially reversed the thymic atrophy and decreased the number of CD4⁺CD8⁺ thymocytes without affecting parasitemia and the number of inflammatory foci in the heart. However, tumor necrosis factor- blood levels were increased in infected mice of both strains treated with RU486. Furthermore, the blockade of glucocorticoid receptors accelerated death in C57Bl/6J mice and increased lethality to 100% in Balb/c mice. The results obtained represent the first evidence that an endocrine host response that is coupled to the immune process can strongly affect the course of a parasite infection.