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Regulation of the inflammatory immune response by the cytokine/chemokine network in amoebiasis
Author(s) -
GARCÍAZEPEDA E. A.,
ROJASLÓPEZ A.,
ESQUIVELVELÁZQUEZ M.,
OSTOASALOMA P.
Publication year - 2007
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.1365-3024.2007.00990.x
Subject(s) - entamoeba histolytica , immunology , immune system , amoebiasis , biology , chemokine , amoebic liver abscess , cytokine , naegleria fowleri , liver abscess , meningoencephalitis , genetics , abscess
SUMMARY Amoebiasis is caused by the protozoa Entamoeba histolytica and persists as one of the leading parasitic diseases affecting millions worldwide. This parasite invades the intestinal mucosa, causing amoebic colitis and ulcers. It may also spread to other organs, mainly the liver, causing amoebic liver abscess (ALA). Current research efforts have focused on the development of specific diagnostic tests and animal models searching for a better understanding of the complex physiopathology of this disease. Analysis of the inflammatory immune response during intestinal amoebiasis in both human disease and animal murine models has revealed an important regulatory role for chemokines and cytokines. Recruitment and activation of inflammatory cells can also be modulated by specific protease‐mediated cleavage of cytokines and by secreted amoebic factors such as amoebapores and monocyte locomotion inhibitory factor (MLIF). Unlike intestinal amoebiasis, analysis of the immune response in ALA has mainly been done in the hamster model. This has limited our information regarding the immune response during this phase of the disease. However, even with these limitations, several Th1/2 cytokines, such as IL‐6 and IL‐4, and regulatory cytokines, like IL‐10 and TGFβ, have been associated to the development of this disease.