Abstract
During amoebic liver abscess (ALA) formation in susceptible animals, immune response is regulated by prostaglandin E2 (PGE2) dependent mechanisms. The aim of this study was to analyze the effect of misoprostol (MPL), a PGE1 analogue, on ALA formation in BALB/c mice. Male mice from BALB/c strain were intrahepatically infected with 7.5 × 105 trophozoites of E. histolytica strain HM1:IMSS and treated with 10−4 M of MPL daily until sacrifice at 2, 4, and 7 days postinfection (p.i.). ALA formation was evaluated at 2, 4, and 7 days postinfection; trophozoite morphology was analyzed using immunohistochemistry and image analysis. Results showed an increase in frequency of ALA formation in infected and MPL-treated mice only at 2 days p.i. (P = 0.03). A significant diminution in the size of trophozoites was detected in abscesses from mice independently of MPL treatment (from 5.8 ± 1.1 µm at 2 days p.i. to 2.7 ± 1.9 µm at 7 days p.i.) compared with trophozoites dimensions observed in susceptible hamsters (9.6 ± 2.7 µm) (P < 0.01). These results suggest that MPL treatment may modify the adequate control of inflammatory process to allow the persistence of trophozoites in the liver; however, natural resistance mechanisms cannot be discarded.
Highlights
Amoebic liver abscess (ALA), produced by Entamoeba histolytica infection, is a common complication of invasive intestinal amoebiasis
The increase in Prostaglandin E2 (PGE2) plasmatic levels and induction of the type 2 cyclooxygenase enzyme (COX-2) in infected liver, as well as the expression of COX-2 mRNA in macrophages and neutrophils, was reported by our group using the hamster, a susceptible experimental model [6, 7]. In these studies we found that the inhibition of PGE2 biosynthesis by indomethacin treatment had a beneficial effect limiting the inflammatory process [6]
Gelfoam was obtained from Upjohn (Kalamazoo, MI, USA); suture 3/0 Curex was obtained from International Pharmaceutics (Mexico); formalin and hematoxylin and eosin (H&E) were obtained from Merck (Darmstadt, Germany)
Summary
Amoebic liver abscess (ALA), produced by Entamoeba histolytica infection, is a common complication of invasive intestinal amoebiasis. Studies done in SCID mice in which a human intestinal xenograft was implanted have provided evidence that the infection with E. histolytica promotes an intense acute inflammatory reaction, accomplished by neutrophil infiltration with an increase in PGE2-COX-2 enzyme dependent levels [8]. These results suggest that PGE2 could be a host-dependent factor involved
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