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Expression of cytokines and their regulation during amoebic liver abscess development
Author(s) -
PACHECOYÉPEZ J.,
GALVÁNMOROYOQUI J. M.,
MEZA I.,
TSUTSUMI V.,
SHIBAYAMA M.
Publication year - 2011
Publication title -
parasite immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.795
H-Index - 75
eISSN - 1365-3024
pISSN - 0141-9838
DOI - 10.1111/j.1365-3024.2010.01252.x
Subject(s) - amoebic liver abscess , entamoeba histolytica , biology , liver abscess , immunology , tumor necrosis factor alpha , proinflammatory cytokine , peripheral blood mononuclear cell , macrophage , inflammation , pathology , abscess , medicine , in vitro , biochemistry , genetics
Summary Amoebic liver abscess (ALA) is the most important extraintestinal complication of Entamoeba histolytica infection. Amoebic liver abscess development causes severe destruction of the liver tissue concomitant with a strong inflammatory reaction. We analyse the in situ expression of TNF‐α, IFN‐γ, IL‐1β, 1L‐8 and IL‐10 at different stages of ALA development in a susceptible animal model. Results showed that after inoculation, neutrophils (PMN) and some macrophages infiltrated the liver and were positive for TNF‐α and IFN‐γ at the acute phase of amoeba infection. The presence of these cytokines was transient and decreased as tissue damage progressed. In contrast, IL‐1β and IL‐8 were detected mainly in neutrophils and macrophages from the periods of acute infection to subacute and chronic infection and decreased when granulomas were formed. The IL‐10 was expressed in PMN and mononuclear cells and only during a short period at the onset of acute infection. The qRT‐PCR of mRNA revealed a relationship with the expression of the cytokines in cells found in the ALA. Furthermore, our data suggest that IL‐10 does not regulate local production of these cytokines. Our results indicate that an exacerbated inflammatory milieu is established and contributes to liver tissue damage and probably supports the survival of the parasites.