Prostaglandin and nitric oxide regulate TNF-α production during Trypanosoma cruzi infection

被引:38
作者
Borges, MM [1 ]
Kloetzel, JK
Andrade, HF
Tadokoro, CE
Pinge, P
Abrahamsohn, I
机构
[1] Inst Butantan, Lab Imunoquim, Sao Paulo, Brazil
[2] Inst Trop Med, BR-0540300 Sao Paulo, Brazil
[3] Univ Sao Paulo, Inst Ciencias Biomed, Dept Parasitol, Sao Paulo, Brazil
[4] Univ Sao Paulo, Inst Ciencias Biomed, Dept Imunol, Sao Paulo, Brazil
基金
巴西圣保罗研究基金会;
关键词
Trypanosoma cruzi; macrophage; TNF-alpha; prostaglandins; nitric oxide;
D O I
10.1016/S0165-2478(98)00034-0
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
The mechanisms that control TNF-alpha production by macrophages during Trypanosoma cruzi infection are still unknown. Destruction of intracellular forms by cytokine activated macrophages is considered to be a major mechanism of parasite elimination. Although in vitro TNF-alpha contributes to enhanced parasite destruction by macrophages, previous work in vivo has shown that as the parasite burden increases, serum TNF-alpha levels decline. In this report we show that TNF-alpha production by peritoneal adherent cells is elevated at the initial phase of T. cruzi infection. As infection progresses TNF-alpha production decreases. The observed reduction is partly due to inhibition, largely exerted by endogenous PG and secondarily by NO. Inhibition of their synthesis partially restored the ability to produce high levels of TNF-alpha to macrophages upon stimulation by LPS. Neither endogenous IL-10 nor TGF-beta seem to be involved in the negative regulation of TNF-alpha production. (C) 1998 Elsevier Science B.V. All rights reserved.
引用
收藏
页码:1 / 8
页数:8
相关论文
共 35 条
[11]   LACK OF PROTECTION AGAINST TRYPANOSOMA-CRUZI BY MULTIPLE DOSES OF TRYPANOSOMA-LEWISI CULTURE FORMS - DISCUSSION ON SOME STRAINS OF LEWISI [J].
DEANE, MP ;
KLOETZEL, J .
EXPERIMENTAL PARASITOLOGY, 1974, 35 (03) :406-410
[12]  
DETITTO EH, 1986, J IMMUNOL, V137, P1342
[13]  
DING AH, 1988, J IMMUNOL, V141, P2407
[14]   COMPARISON OF INVITRO-CELL CYTO-TOXIC ASSAYS FOR TUMOR NECROSIS FACTOR [J].
FLICK, DA ;
GIFFORD, GE .
JOURNAL OF IMMUNOLOGICAL METHODS, 1984, 68 (1-2) :167-175
[15]   RELATIONSHIP BETWEEN GRANULOCYTE MACROPHAGE-COLONY-STIMULATING FACTOR, TUMOR-NECROSIS-FACTOR-ALPHA AND TRYPANOSOMA-CRUZI INFECTION OF MURINE MACROPHAGES [J].
FONTT, EO ;
VRAY, B .
PARASITE IMMUNOLOGY, 1995, 17 (03) :135-141
[16]   THE MICROBICIDAL ACTIVITY OF INTERFERON-GAMMA-TREATED MACROPHAGES AGAINST TRYPANOSOMA-CRUZI INVOLVES AN L-ARGININE-DEPENDENT, NITROGEN OXIDE-MEDIATED MECHANISM INHIBITABLE BY INTERLEUKIN-10 AND TRANSFORMING GROWTH-FACTOR-BETA [J].
GAZZINELLI, RT ;
OSWALD, IP ;
HIENY, S ;
JAMES, SL ;
SHER, A .
EUROPEAN JOURNAL OF IMMUNOLOGY, 1992, 22 (10) :2501-2506
[17]   TRYPANOSOMA-CRUZI - CYTOKINE EFFECTS ON MACROPHAGE TRYPANOCIDAL ACTIVITY [J].
GOLDEN, JM ;
TARLETON, RL .
EXPERIMENTAL PARASITOLOGY, 1991, 72 (04) :391-402
[18]  
HASS JG, 1990, P NATL ACAD SCI USA, V87, P9563
[19]  
HOFT DF, 1993, J IMMUNOL, V151, P7038
[20]   Interleukin-12-mediated resistance to Trypanosoma cruzi is dependent on tumor necrosis factor alpha and gamma interferon [J].
Hunter, CA ;
Slifer, T ;
Araujo, F .
INFECTION AND IMMUNITY, 1996, 64 (07) :2381-2386