Nitric oxide interaction with IL-10, MIP-1α, MCP-1 and RANTES over the in vitro granuloma formation against different Schistosoma mansoni antigenic preparations on human schistosomiasis

被引:9
作者
Oliveira, DM
Silva-Teixeira, DN
Gustavson, S
Oliveira, SMP
Goes, AM
机构
[1] Univ Fed Minas Gerais, Inst Ciencias Biol, Dept Bioquim & Imunol, BR-30161970 Belo Horizonte, MG, Brazil
[2] Univ Estadual Ceara, Fac Vet, Dept Vet Med, UECE, BR-60740000 Fortaleza, Ceara, Brazil
[3] Univ Fed Ceara, Ctr Ciencias Agr, Dept Zootecnia, BR-60021970 Fortaleza, Ceara, Brazil
关键词
nitric oxide; IL-10; MIP-1; alpha; MCP-1; RANTES; in vitro granuloma; schistosomiasis;
D O I
10.1017/S0031182099005636
中图分类号
R38 [医学寄生虫学]; Q [生物科学];
学科分类号
07 ; 0710 ; 09 ; 100103 ;
摘要
Nitric oxide (NO) produced by cytokine-activated macrophages is reported to be cytotoxic against the helminth Schistosoma mansoni, although this is a controversial issue. Previous work in our laboratory identified a fraction of S. mansoni soluble adult worm antigenic preparation (SWAP), named PIII, able to elicit significant in vitro cell proliferation and at the same time lower in vitro and in vivo granuloma formation when compared either to soluble egg antigen (SEA) or to SWAP. Here we report that, in comparison to other S. mansoni antigenic preparations (SEA and SWAP), supernatants of PBMC cultivated with PIII possess higher concentrations of interleukin-10 (IL-10) and macrophage inflammatory protein (MIP-1 alpha), concomitantly with lower concentrations of monocyte chemoattractant protein (MCP-1) and regulated on activation, normal T expressed and secreted (RANTES). In the particular case of NO inhibition, supernatants of PBMC cultivated with PIII present decreased IL-10 levels. Altogether, these results indicate that IL-10, MIP-1 alpha, MCP-1 and RANTES are distinctively important elements in the PIII modulating role, while NO seems to be pivotal in the regulation of granulomatous responses.
引用
收藏
页码:391 / 398
页数:8
相关论文
共 25 条
[1]  
BERKMAN N, 1995, J IMMUNOL, V155, P4412
[2]  
BRADFORD MM, 1976, ANAL BIOCHEM, V72, P248, DOI 10.1016/0003-2697(76)90527-3
[3]  
Chensue SW, 1996, J IMMUNOL, V157, P4602
[4]  
Chensue SW, 1997, J IMMUNOL, V159, P3565
[5]  
DOUGHTY B L, 1987, Memorias do Instituto Oswaldo Cruz, V82, P47, DOI 10.1590/S0074-02761987000800009
[6]  
DOUGHTY BL, 1984, J IMMUNOL, V133, P993
[7]   INTERFERON-GAMMA AND TUMOR NECROSIS FACTOR INDUCE THE L-ARGININE-DEPENDENT CYTO-TOXIC EFFECTOR MECHANISM IN MURINE MACROPHAGES [J].
DRAPIER, JC ;
WIETZERBIN, J ;
HIBBS, JB .
EUROPEAN JOURNAL OF IMMUNOLOGY, 1988, 18 (10) :1587-1592
[8]  
FIORENTINO DF, 1991, J IMMUNOL, V147, P3815
[9]   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
[10]  
Green T. R. G., 1982, Behaviour and Information Technology, V1, P3, DOI 10.1080/01449298208914433