Macrophage lipid body induction by Chagas disease in vivo: putative intracellular domains for eicosanoid formation during infection

被引:87
作者
Melo, RCN [1 ]
D'Avila, H
Fabrino, DL
Almeida, PE
Bozza, PT
机构
[1] Univ Fed Juiz de Fora, Dept Biol, Lab Cellular Biol, BR-36036330 Juiz De Fora, MG, Brazil
[2] Inst Oswaldo Cruz, Dept Physiol & Pharmacodynam, Lab Immunopharmacol, BR-20001 Rio De Janeiro, Brazil
关键词
Chagas disease; lipid bodies; macrophages; myocarditis; ultrastructure; prostaglandins;
D O I
10.1016/S0040-8166(02)00105-2
中图分类号
R602 [外科病理学、解剖学]; R32 [人体形态学];
学科分类号
100101 ;
摘要
Lipid bodies (LB), lipid-rich inclusions abundantly present in cells engaged in inflammation, are specialized intracellular domains involved in generating inflammatory mediators, the eicosanoids. Since the acute Trypanosoma cruzi infection triggers A potent inflammatory reaction characterized by a great increase of peripheral blood monocyte (PBM) and macrophage numbers, we investigated the LB occurrence in these cells. The experimental rat infection by T cruzi (Y strain) induced significant increase of the LB numbers in peritoneal macrophages at day 6 and 12, accompanied by significant enhancement of Prostaglandin E-2 (PGE(2)) production, as measured by EIA. At day 12, ultrastructural analysis of the heart, a target organ of the disease, showed numerous macrophages with LB prominently increased in number (mean of 8.3 per section view, range of 1-25) compared to controls (mean of 2.6 per section view, range of 0-3) and size. PBM from all groups rarely showed LB. Our results demonstrate, for the first time, that T cruzi infection in rats elicits important LB formation in inflammatory macrophages but not in PBM. The increase in LB numbers during infection positively correlates with increased generation of PGE(2), suggesting that LB may have a role in the heightened eicosanoid production observed during T cruzi infection. (C) 2003 Elsevier Science Ltd. All rights reserved.
引用
收藏
页码:59 / 67
页数:9
相关论文
共 46 条
[1]   TOLUIDINE BLUE-BASIC FUCHSIN STAIN FOR GLYCOLMETHACRYLATE EMBEDDED TISSUE [J].
ABREU, MA ;
BAROZA, LGV ;
ROSSI, MA .
JOURNAL OF HISTOTECHNOLOGY, 1993, 16 (02) :139-140
[2]   The haematology of Trypanosoma congolense infection in cattle .2. Macrophage structure and function in the bone marrow of Boran cattle [J].
Anosa, VO ;
LoganHenfrey, LL ;
Wells, CW .
COMPARATIVE HAEMATOLOGY INTERNATIONAL, 1997, 7 (01) :23-29
[3]   The cellular biology of eosinophil eicosanoid formation and function [J].
Bandeira-Melo, C ;
Bozza, PT ;
Weller, PF .
JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, 2002, 109 (03) :393-400
[4]   Extranuclear lipid bodies, elicited by CCR3-mediated signaling pathways, are the sites of chemokine-enhanced leukotriene C4 production in eosinophils and basophils [J].
Bandeira-Melo, C ;
Phoofolo, M ;
Weller, PF .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2001, 276 (25) :22779-22787
[5]   ULTRASTRUCTURAL IMMUNOGOLD LOCALIZATION OF SUBCELLULAR SITES OF TNF-ALPHA IN COLONIC CROHNS-DISEASE [J].
BEIL, WJ ;
WELLER, PF ;
PEPPERCORN, MA ;
GALLI, SJ ;
DVORAK, AM .
JOURNAL OF LEUKOCYTE BIOLOGY, 1995, 58 (03) :284-298
[6]   Prostaglandin and nitric oxide regulate TNF-α production during Trypanosoma cruzi infection [J].
Borges, MM ;
Kloetzel, JK ;
Andrade, HF ;
Tadokoro, CE ;
Pinge, P ;
Abrahamsohn, I .
IMMUNOLOGY LETTERS, 1998, 63 (01) :1-8
[7]   Eosinophil lipid bodies: Specific, inducible intracellular sites for enhanced eicosanoid formation [J].
Bozza, PT ;
Yu, WG ;
Penrose, JF ;
Morgan, ES ;
Dvorak, AM ;
Weller, PF .
JOURNAL OF EXPERIMENTAL MEDICINE, 1997, 186 (06) :909-920
[8]   Leukocyte lipid body formation and eicosanoid generation: Cyclooxygenase-independent inhibition by aspirin [J].
Bozza, PT ;
Payne, JL ;
Morham, SG ;
Langenbach, R ;
Smithies, O ;
Weller, PF .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1996, 93 (20) :11091-11096
[9]   Mechanisms of platelet-activating factor-induced lipid body formation: Requisite roles for 5-lipoxygenase and de novo protein synthesis in the compartmentalization of neutrophil lipids [J].
Bozza, PT ;
Payne, JL ;
Goulet, JL ;
Weller, PF .
JOURNAL OF EXPERIMENTAL MEDICINE, 1996, 183 (04) :1515-1525
[10]   Pathways for eosinophil lipid body induction: differing signal transduction in cells from normal and hypereosinophilic subjects [J].
Bozza, PT ;
Yu, WG ;
Cassara, J ;
Weller, PF .
JOURNAL OF LEUKOCYTE BIOLOGY, 1998, 64 (04) :563-569