Role of Prostaglandin E2 on Amoebic Liver Abscess Formation in Hamsters

Abstract

Entamoeba histolytica can modulate macrophage functions and cytokine production by a prostaglandin E₂ (PGE₂) mechanism. To study the participation of PGE₂ on amoebic liver abscess formation, we tested the effect of the PG synthesis inhibitor indomethacin (INDO) on abscess development in hamsters infected intrahepatically with E. histolytica trophozoites. Male infected animals had higher levels of plasma PGE₂ (5.7 ± 0.7 pg/ml pre-infection; 26.0 ± 2.0 pg/ml 7 days postinfection; p < 0.001). INDO prevented this increase, so that infected-treated and control non-infected animals had similar levels of plasma PGE₂. INDO reduced liver and abscess weight by 18% and 30% respectively (p < 0.05). Cyclooxygenase (COX) activity determination by thin layer chromatography using (1-¹⁴C) arachidonic acid (AA) showed that liver microsomes from infected animals produced more PGE₂ than controls. COX activity was considerably inhibited in infected INDO-treated animals. Our data suggest that E. histolytica can stimulate the hepatic production of PGE₂ which contributes to pathogenesis of amoebic abscesses through generation and support of the inflammation. The partial effect of INDO treatment suggests that additional factors are involved.