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

• Published in: Experimental parasitology 2008-04, Vol.118 (4), p.514-521
• Main Authors: Abdalla, G.K., Faria, G.E.L., Silva, K.T., Castro, E.C.C., Reis, M.A., Michelin, M.A.
• Format: Article
• Language: English
• Subjects: Acute Disease; Animals; Biological and medical sciences; bovine serum albumin; BSA; Cardiac lesions; Cells, Cultured; Chagas Disease - drug therapy; Chagas Disease - immunology; Chagas Disease - pathology; COX; COX-2; cyclooxygenase; Cyclooxygenase 1 - analysis; Cyclooxygenase 2 - analysis; Cyclooxygenase Inhibitors - therapeutic use; Cytokines; degree Celsius; Dinoprostone - biosynthesis; Dinoprostone - physiology; Fibrosis; Fundamental and applied biological sciences. Psychology; hematoxylin–eosin; hour; IFN-γ; immunoglobulin; interferon γ; interleukin; Life cycle. Host-agent relationship. Pathogenesis; major histocompatibility complex; Male; mg/kg; MHC; Mice; Mice, Inbred BALB C; micro Currier; micrograms per milliliter; milligrams per kilogram; Myocardium - enzymology; Myocardium - pathology; nanograms per milliliter; ng/ml; nitric oxide; Parasitemia - drug therapy; Parasitemia - parasitology; PBS; PGE 2; phosphate buffered saline; Prostaglandin; prostaglandin E 2; Prostaglandins - analysis; Protozoa; Pyridines - therapeutic use; Spleen - chemistry; Spleen - cytology; Sulfones - therapeutic use; T helper; T. cruzi; Thiazines - therapeutic use; Thiazoles - therapeutic use; TNF-α; Trypanosoma cruzi; Trypanosoma cruzi - immunology; tumor necrosis factor α; μCi; μg/ml
• ISSN: 0014-4894; 1090-2449
• DOI: 10.1016/j.exppara.2007.11.003

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 × 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 21st 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.