Base de dados : HANSEN
Pesquisa : FATOR DE NECROSE TUMORAL ALFA/BI [Descritor de assunto]
Referências encontradas : 4 [refinar]
Mostrando: 1 .. 4   no formato [Detalhado]

página 1 de 1

  1 / 4 HANSEN  
              next record last record
seleciona
para imprimir
Texto Completo-en
Id:26989
Autor:Shimizu, Toshiaki; Maw, Win Win; Tomioka, Haruaki.
Título:Roles of tumor necrosis factor-alpha and transforming growth factor-beta in regulating intercellular adhesion molecule-1 expression on murine peritoneal macrophages infected with M. Leprae.
Fonte:Int. J. Lepr;67(1):36-45, Mar., 1999. tab, graf.
Resumo:Profiles of intercellular adhesion molecule-1 (ICAM-1) expression on murine peritoneal macrophages (M phi s) infected with Mycobacterium leprae during cultivation were examined with special reference to the regulatory effects of tumor necrosis factor-alpha (TNF-alpha) and transforming growth factor-beta (TGF-beta). When M phi s were infected with M. leprae or stimulated with heat-killed M. leprae at day 0, their ICAM-1 expression, measured in terms of the ratio of M phi s positively stained with anti-ICAM-1 antibody (Ab), rapidly increased, peaking during days 1 to 3 and thereafter fell, returning to the normal level by day 7. The addition of TNF-alpha or anti-TGF-beta Ab inhibited the middle phase (day 7) downregulation of M phi ICAM-1 expression, although the late-phase (day 14) downregulation of ICAM-1 was not prevented by them. M. leprae-infected M phi s released small amounts of TNF-alpha and significant amounts of TGF-beta into the culture medium. This may indicate that M. leprae-infected M phi s produced the majority of TNF-alpha in a membrane-bound form. Alternatively, endogenous TNF-alpha might upregulate M phi ICAM-1 expression even at very low concentrations. In any case, these findings indicate the central roles of TNF-alpha and TGF-beta in the early phase upregulation and the middle-to-late phase downregulation, respectively, of ICAM-1 expression by M. leprae-infected M phi s. (AU)^ien.
Descritores:Fator de Necrose Tumoral alfa/imunol
Fator de Necrose Tumoral alfa/fisiol
Macrófagos/imunol
Macrófagos/microbiol
Mycobacterium leprae/imunol
Mycobacterium leprae/fisiol
Meio Eletrônico:http://hansen.bvs.ilsl.br/textoc/revistas/intjlepr/1999/pdf/v67n1/v67n1a06.pdf - en.
Localização:BR191.1


  2 / 4 HANSEN  
              first record previous record next record last record
seleciona
para imprimir
Texto Completo-en
Id:26740
Autor:Park, Eunkyue; Schuller-Levis, Georgia; Park, Seung Yong; Jia, Jun Hua; Levis, William R.
Título:Pentoxifylline downregulares nitric oxide and tumor necrosis factor-a induced by mycobacterial lipoarabinomannan in a macrophage cell line.
Fonte:Int. J. Lepr;69(3):225-233, Sept., 2001. ilus, tab, graf.
Resumo:Pentoxifylline (PTX), a phosphodiesterase inhibitor, is known to downregulate tumor necrosis factor-alpha (TNF-alpha) secretion induced by lipopolysacchride (LPS) and gamma interferon (IFN-gamma). We have had limited success in treating leprosy reactions, including erythema nodosum leprosum (ENL), in which TNF-alpha has been identified as a major proinflammatory cytokine. PTX inhibited production of NO (IC50 approximately equal to 1.0 mg/ml) and TNF-alpha (IC50 approximately equal to 0.05 mg/ml) in a dose-dependent fashion. As little as 0.5 mg/ml of PTX decreased NO production and 0.01 mg/ml of PTX inhibited TNF-alpha production. Western blot analyses demonstrated that iNOS was suppressed by PTX. Northern blot analyses showed significant reduction of TNF-alpha mRNA. We conclude that PTX is an effective inhibitor of lipoarabinomannan (LAM)-induced TNF-alpha production at both the product and transcriptional levels in our macrophage cell line. PTX also showed moderate inhibition of NO at the product level as well as translation of iNOS. (AU)^ien.
Descritores:Pentoxifilina/sint quim
Pentoxifilina/imunol
Fator de Necrose Tumoral alfa/sint quim
Fator de Necrose Tumoral alfa/imunol
Macrófagos/imunol
Meio Eletrônico:http://hansen.bvs.ilsl.br/textoc/revistas/intjlepr/2001/pdf/v69n3/v69n3a07.pdf - en.
Localização:BR191.1


  3 / 4 HANSEN  
              first record previous record next record last record
seleciona
para imprimir
Id:23971
Autor:Scollard, D. M; Joyce M. P; Gillis, T. P
Título:Development of leprosy and type 1 leprosy reactions after treatment with infliximab: a report of 2 cases
..-
Fonte:s.l; s.n; 2006. 4 p. ilus.
Resumo:Humanized monoclonal antibodies to tumor necrosis factor- alpha are valuable for the treatment of rheumatologic conditions, but they have been associated with the development of serious infections. We report the first 2 cases of leprosy developing after treatment with infliximab. After discontinuation of infliximab, both patients developed type 1 ([quot ]reversal[quot ]) leprosy reactions. (AU).
Descritores:Anticorpos Monoclonais/*AE/IM/TU
Anti-Reumáticos/*AE/IM/TU
Artrite/*DT
Glucocorticóides/TU
Hansenostáticos/TU
Hanseníase Dimorfa/CI/*ET/MI
Fator de Necrose Tumoral alfa/AI
Limites:HUMANO
MASCULINO
FEMININO
MEIA-IDADE
IDOSO
SUPPORT, U.S. GOV'T, NON-P.H.S.
Localização:BR191.1; 09363/S


  4 / 4 HANSEN  
              first record previous record
seleciona
para imprimir
Id:23197
Autor:Kang, Tae Jin; Yeum, Chung Eun; Kim, Byoung Chul; You, Eun-Young; Chae, Gue-Tae
Título:Differential production of interleukin-10 and interleukin-12 in mononuclear cells from leprosy patients with a Toll-like receptor 2 mutation
..-
Fonte:s.l; s.n; 2004. 7 p. ilus, tab, graf.
Resumo:Toll-like receptor 2 (TLR2) is a key mediator of the immune response to mycobacterial infections, and mutations in TLR2 have been shown to confer susceptibility to infection with mycobacteria. This study investigated the profiles of cytokines, such as interferon (IFN)-gamma, interleukin (IL)-10, IL-12 and tumour necrosis factor (TNF)-alpha in response to Mycobacterium leprae in peripheral blood mononuclear cells (PBMC) with the TLR2 mutation Arg677Trp, a recently reported polymorphism that is associated with lepromatous leprosy. In leprosy patients with the TLR2 mutation, production of IL-2, IL-12, IFN-gamma, and TNF-alpha by M. leprae-stimulated PBMC were significantly decreased compared with that in groups with wild-type TLR2. However, the cells from patients with the TLR2 mutation showed significantly increased production of IL-10. There was no significant difference in IL-4 production between the mutant and wild-type during stimulation. Thus, these results suggest that the TLR2 signal pathway plays a critical role in the alteration of cytokine profiles in PBMC from leprosy patients and the TLR2 mutation Arg677Trp provides a mechanism for the poor cellular immune response associated with lepromatous leprosy. (AU).
Descritores:Sequência de Bases
Interleucina-10/*BI
Interleucina-12/*BI
Hanseníase/GE/*IM
Leucócitos Mononucleares/IM
Glicoproteínas de Membrana/*GE/ME
Camundongos Nus
Dados de Sequência Molecular
Mutação Puntual/*
Receptores da Superfície Celular/*GE/ME
Receptor 2 Toll-Like
Receptores Toll-Like
Fator de Necrose Tumoral alfa/BI
Limites:Adulto
Idoso
Animais
Feminino
Humanos
Masculino
Camundongos
Research Support, Non-U.S. Gov't
Meia-Idade
Localização:BR191.1; 09341/s



página 1 de 1
   


Refinar a pesquisa
  Base de dados : HANSEN Formulário avançado   
Pesquisar por : Formulário livre   

    Pesquisar no campo  
1  
2
3
 
           



Search engine: iAH v2.6.1 powered by WWWISIS

BIREME/PAHO/WHO - Latin American and Caribbean Center on Health Sciences Information