title: Trypanosoma cruzi: the role of PGE2 in immune response during the acute phase of experimental infection.
abstract: 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 (1x10(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.
authors.affiliation: Laboratory of Immunology, Federal University of Triângulo Mineiro, Rua Frei Paulino, 30, 38 025-180 Uberaba, MG, Brazil.
authors.forename: G K
authors.initials: GK
authors.lastname: Abdalla
authors.forename: G E L
authors.initials: GE
authors.lastname: Faria
authors.forename: K T
authors.initials: KT
authors.lastname: Silva
authors.forename: E C C
authors.initials: EC
authors.lastname: Castro
authors.forename: M A
authors.initials: MA
authors.lastname: Reis
authors.forename: M A
authors.initials: MA
authors.lastname: Michelin
mesh_terms: D000208:Acute Disease; D000818:Animals; D002478:Cells, Cultured; D014355:Chagas Disease / Q000188:drug therapy / Q000276:immunology* / Q000473:pathology; D051545:Cyclooxygenase 1 / Q000032:analysis; D051546:Cyclooxygenase 2 / Q000032:analysis; D016861:Cyclooxygenase Inhibitors / Q000627:therapeutic use; D015232:Dinoprostone / Q000096:biosynthesis / Q000502:physiology*; D000077613:Etoricoxib; D005355:Fibrosis; D008297:Male; D000077239:Meloxicam; D051379:Mice; D008807:Mice, Inbred BALB C; D009206:Myocardium / Q000201:enzymology / Q000473:pathology; D018512:Parasitemia / Q000188:drug therapy / Q000469:parasitology; D011453:Prostaglandins / Q000032:analysis; D011725:Pyridines / Q000627:therapeutic use; D013154:Spleen / Q000737:chemistry / Q000166:cytology; D013450:Sulfones / Q000627:therapeutic use; D013843:Thiazines / Q000627:therapeutic use; D013844:Thiazoles / Q000627:therapeutic use; D014349:Trypanosoma cruzi / Q000276:immunology*
chemical_list: D016861:Cyclooxygenase Inhibitors; D011453:Prostaglandins; D011725:Pyridines; D013450:Sulfones; D013843:Thiazines; D013844:Thiazoles; D051545:Cyclooxygenase 1; D051546:Cyclooxygenase 2; D015232:Dinoprostone; D000077239:Meloxicam; D000077613:Etoricoxib