Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 2 de 2
Filtrar
Mais filtros











Base de dados
Intervalo de ano de publicação
1.
J Immunol ; 175(4): 2563-9, 2005 Aug 15.
Artigo em Inglês | MEDLINE | ID: mdl-16081830

RESUMO

Infection with gastrointestinal nematodes exerts profound effects on both immune and physiological responses of the host. Helminth infection induces a hypercontractility of intestinal smooth muscle that is dependent on the Th2 cytokines, IL-4 and IL-13, and may contribute to worm expulsion. Protease-activated receptors (PARs) are expressed throughout the gut, and activation of PAR-1 was observed in asthma, a Th2-driven pathology. In the current study we investigated the physiologic and immunologic regulation of PAR-1 in the murine small intestine, specifically 1) the effect of PAR-1 agonists on small intestinal smooth muscle contractility, 2) the effects of Nippostrongylus brasiliensis infection on PAR-1 responses, 3) the roles of IL-13 and IL-4 in N. brasiliensis infection-induced alterations in PAR-1 responses, and 4) the STAT6 dependence of these responses. We demonstrate that PAR-1 activation induces contraction of murine intestinal smooth muscle that is enhanced during helminth infection. This hypercontractility is associated with an elevated expression of PAR-1 mRNA and protein. N. brasiliensis-induced changes in PAR-1 function and expression were seen in IL-4-deficient mice, but not in IL-13- or STAT6-deficient mice, indicating the dependence of IL-13 on the STAT6 signaling pathway independent of IL-4.


Assuntos
Jejuno/imunologia , Jejuno/metabolismo , Nippostrongylus/imunologia , Receptor PAR-1/biossíntese , Infecções por Strongylida/imunologia , Infecções por Strongylida/metabolismo , Animais , Relação Dose-Resposta a Droga , Feminino , Interleucina-13/administração & dosagem , Interleucina-13/deficiência , Interleucina-13/fisiologia , Interleucina-4/deficiência , Interleucina-4/genética , Interleucina-4/fisiologia , Jejuno/efeitos dos fármacos , Jejuno/parasitologia , Camundongos , Camundongos Endogâmicos BALB C , Camundongos Knockout , Contração Muscular/efeitos dos fármacos , Músculo Liso/efeitos dos fármacos , Músculo Liso/fisiologia , Oligopeptídeos/farmacologia , Receptor PAR-1/agonistas , Receptor PAR-1/metabolismo , Fator de Transcrição STAT6/deficiência , Fator de Transcrição STAT6/genética , Fator de Transcrição STAT6/fisiologia , Regulação para Cima/imunologia
2.
Immunity ; 8(2): 255-64, 1998 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-9492006

RESUMO

Although IL-4 induces expulsion of the gastrointestinal nematode parasite, Nippostrongylus brasiliensis, from immunodeficient mice, this parasite is expelled normally by IL-4-deficient mice. This apparent paradox is explained by observations that IL-4 receptor alpha chain (IL-4Ralpha)-deficient mice and Stat6-deficient mice fail to expel N. brasiliensis, and a specific antagonist for IL-13, another activator of Stat6 through IL-4Ralpha, prevents worm expulsion. Thus, N. brasiliensis expulsion requires signaling via IL-4Ralpha and Stat6, and IL-13 may be more important than IL-4 as an inducer of the Stat6 signaling that leads to worm expulsion. Additional observations made in the course of these experiments demonstrate that Stat6 signaling is not required for IL-4 enhancement of IgG1 production and actually inhibits IL-4-induction of mucosal mastocytosis.


Assuntos
Gastroenteropatias/imunologia , Interleucina-13/deficiência , Nippostrongylus/imunologia , Receptores de Interleucina-4/deficiência , Infecções por Strongylida/imunologia , Transativadores/deficiência , Animais , Anticorpos Anti-Helmínticos/biossíntese , Feminino , Gastroenteropatias/parasitologia , Interações Hospedeiro-Parasita/imunologia , Interferon gama/biossíntese , Interleucina-13/genética , Mucosa Intestinal/imunologia , Mastocitose/imunologia , Camundongos , Camundongos Endogâmicos BALB C , Camundongos Endogâmicos C57BL , Camundongos Mutantes , Camundongos Nus , Receptores de Interleucina-4/genética , Fator de Transcrição STAT6 , Transdução de Sinais , Transativadores/genética
SELEÇÃO DE REFERÊNCIAS
DETALHE DA PESQUISA