4.2 Article

Trypanosoma cruzi:: The role of PGE2 in immune response during the acute phase of experimental infection

Journal

EXPERIMENTAL PARASITOLOGY
Volume 118, Issue 4, Pages 514-521

Publisher

ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.exppara.2007.11.003

Keywords

pGE(2); prostaglandin E; IL; interleukin; TNF-alpha; tumor necrosis factor alpha; IFN-gamma; interferon gamma; COX; cyclooxygenase; Th; T helper; T cruzi; Trypanosoma cruzi; Ig; immunoglobulin; NO; nitric oxide; MHC; major histocompatibility complex; PBS; phosphate buffered saline; mu Ci; micro Currier; h; hour; degrees C; degree Celsius-; mu g/ml; micrograms per milliliter; BSA; bovine serum albumin; HE; hematoxylin-eosin; mg/kg; milligrams per kilogram; ng/ml; nanograms per milliliter; Prostaglandin; Cytokines; Cardiac lesions; COX-2

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Chagas disease is characterized by cardiac lesions and a high level of PGE2. Our objective was to investigate the role of PGE2 in cardiac lesions. BALB/c, mice were infected with Trypanosoma CruZi (1 X 10(3) trypomastigote forms) and were treated daily with PBS, meloxicam (0.5 mg/kg) or etoricoxib (0.6 mg/kg). The animals were sacrificed on the 21 st day of infection and we collected the cardiac tissue and spleen cells for tissue culture. We observed that treatment with COX-2 inhibitors was able to decrease synthesis of PGE2 by spleen cells. This reduction was accompanied by reduction of the inflammatory infiltrate, parasite nets, cardiac fibrosis and fewer COX-2 positive cells in cardiac tissue obtained from these animals. In conclusion, treatment with COX-2 inhibitors, and consequent inhibition of PGE2 synthesis, was able to reduce the cardiac damage observed during the acute phase of experimental Chagas disease, thus demonstrating the involvement of this mediator in the cardiac lesion. (c) 2007 Elsevier Inc. All rights reserved.

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