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
[1]   Trypanosoma cruzi: IL-10, TNF, IFN-gamma, and IL-12 regulate innate and acquired immunity to infection [J].
Abrahamsohn, IA ;
Coffman, RL .
EXPERIMENTAL PARASITOLOGY, 1996, 84 (02) :231-244
[2]  
ABRAHAMSOHN IA, 1995, J IMMUNOL, V155, P3955
[3]  
ALBINA JE, 1993, J IMMUNOL, V150, P5080
[4]  
BLACK CM, 1989, IMMUNOLOGY, V68, P570
[5]  
BOGDAN C, 1992, J BIOL CHEM, V267, P23301
[6]   MACROPHAGE DEACTIVATION BY INTERLEUKIN-10 [J].
BOGDAN, C ;
VODOVOTZ, Y ;
NATHAN, C .
JOURNAL OF EXPERIMENTAL MEDICINE, 1991, 174 (06) :1549-1555
[7]   INTERFERON-GAMMA LEVELS DURING THE COURSE OF TRYPANOSOMA-CRUZI INFECTION OF CALOMYS CALLOSUS (RODENTIA-CRICETIDAE) AND SWISS MICE [J].
BORGES, MM ;
VASSAO, R ;
ANDRADE, SG ;
PEREIRA, CA ;
KLOETZEL, JK .
PARASITOLOGY RESEARCH, 1995, 81 (06) :498-504
[8]   MACROPHAGE ACTIVATION AND HISTOPATHOLOGICAL FINDINGS IN CALOMYS-CALLOSUS AND SWISS MICE INFECTED WITH SEVERAL STRAINS OF TRYPANOSOMA-CRUZI [J].
BORGES, MM ;
DEANDRADE, SG ;
PILATTI, CG ;
DOPRADO, JC ;
KLOETZEL, JK .
MEMORIAS DO INSTITUTO OSWALDO CRUZ, 1992, 87 (04) :493-502
[9]   GAMMA-IFN AND MACROPHAGE RESPIRATORY BURST IN CALOMYS CALLOSUS CHALLENGED WITH TRYPANOSOMA-CRUZI BLOOD-STREAM AND METACYCLIC FORMS [J].
BORGES, MM ;
VASSAO, RC ;
PEREIRA, CA ;
KLOETZEL, JK .
IMMUNOLOGY LETTERS, 1994, 42 (1-2) :81-85
[10]  
BRENER Z., 1962, REV INST MED TROP SAO PAULO, V4, P389