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BioMed Research International
Volume 2015 (2015), Article ID 898467, 7 pages
Research Article

Morphological Findings in Trophozoites during Amoebic Abscess Development in Misoprostol-Treated BALB/c Mice

1Facultad de Ciencias Químicas, Universidad Autónoma de Chihuahua, Circuito No. 1, Nuevo Campus Universitario, 31125 Chihuahua, CHIH, Mexico
2Departamento de Anatomía Patológica del Hospital CIMA, Avenida Hacienda del Valle No. 7120, 31217 Chihuahua, CHIH, Mexico
3Departamento de Infectómica y Patogénesis Molecular, CINVESTAV-IPN, Avenida Instituto Politécnico Nacional 2508, 07360 Mexico, DF, Mexico

Received 24 July 2014; Revised 5 October 2014; Accepted 14 October 2014

Academic Editor: Luis I. Terrazas

Copyright © 2015 Andrés Aceves-Cano et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


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 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. (). A significant diminution in the size of trophozoites was detected in abscesses from mice independently of MPL treatment (from µm at 2 days p.i. to µm at 7 days p.i.) compared with trophozoites dimensions observed in susceptible hamsters (µm) (). 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.