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The effect of Entamoeba histolytica on macrophage functions

Infections with Entamoeba histolytica are associated with impaired cell mediated immunity by an unknown mechanism. Macrophages are the most important cells in host defense against invasive amebiasis. The present study investigated the effect of E. histolytica on macrophage functions. Macrophages isolated from gerbils with amebic liver abscess and naive macrophages exposed to soluble amebic proteins induced profound alteration of eicosanoid formation both in cyclooxygenase and lipoxygenase pathways by enhanced PGE$ sb2$ and LTC$ sb4$ production. TNF-$ alpha$ production by macrophages was altered locally in amebic granulomas and at systemic sites during the infection and in response to amebic proteins stimulation in vitro. PGE$ sb2$ produced by macrophages in response to amebic proteins was involved in the down-regulation of TNF-$ alpha$ production. E. histolytica-induced dysfunction of macrophage cytotoxicity against amebae and tumor cells occurred by suppressing NO and by enhancing PGE$ sb2$ production. Amebic proteins suppressed the induction. of IFN-$ gamma$-induced bone marrow macrophage class II MHC Ia molecule synthesis and I-A$ beta$ mRNA expression by stimulating PGE$ sb2$ production. Taken together, these results demonstrate that E. histolytica induced PGE$ sb2$ production plays a central role in the suppression of macrophage effector and accessory cell functions.

Identiferoai:union.ndltd.org:LACETR/oai:collectionscanada.gc.ca:QMM.41170
Date January 1993
CreatorsWang, Wei
ContributorsChadee, K. (advisor)
PublisherMcGill University
Source SetsLibrary and Archives Canada ETDs Repository / Centre d'archives des thèses électroniques de Bibliothèque et Archives Canada
LanguageEnglish
Detected LanguageEnglish
TypeElectronic Thesis or Dissertation
Formatapplication/pdf
CoverageDoctor of Philosophy (Institute of Parasitology.)
RightsAll items in eScholarship@McGill are protected by copyright with all rights reserved unless otherwise indicated.
Relationalephsysno: 001338485, proquestno: NN87950, Theses scanned by UMI/ProQuest.

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