Format

Send to

Choose Destination
Biomed Res Int. 2015;2015:898467. doi: 10.1155/2015/898467. Epub 2015 May 18.

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

Author information

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

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 × 10(5) 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.

PMID:
26090455
PMCID:
PMC4450255
DOI:
10.1155/2015/898467
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Hindawi Publishing Corporation Icon for PubMed Central
Loading ...
Support Center