Wnt/ß-catenin pathway promotes acute lung injury induced by LPS through driving the Th17 response in mice.
Biochem Biophys Res Commun
; 495(2): 1890-1895, 2018 01 08.
Article
en En
| MEDLINE
| ID: mdl-29246763
ABSTRACT
T helper cell 17 (Th17), one type of CD4+ T cell, plays an important role in regulating the acute lung injury (ALI) inflammatory response. Recent studies showed that Wnt/ß-catenin pathway could modulate the differentiation and the function of CD4+ T cell. However, whether Wnt/ß-catenin could regulate the differentiation and function of Th17 in the development and progress of ALI induced by lipopolysaccharide (LPS) is still unknown. To test this, we used dickkopf1 (Dkk-1) to block the Wnt/ß-catenin pathway and LiCl to activate the Wnt/ß-catenin pathway by instillation to the murine model of ALI. Our results revealed that activation of Wnt/ß-catenin pathway significantly aggravated the LPS-induced lung inflammation. Meanwhile, we observed that activation of Wnt/ß-catenin pathway promoted Th17 response by analyzing CD4+ T cells and the related cytokines secretions. Enhanced Th17 response was responsible for the further neutrophils infiltration and pro-inflammatory cytokines production. In addition, activation of Wnt/ß-catenin pathway resulted in induced expression of retinoic acid related orphan receptor-γt (RORγt) via histone acetyltransferase p300. These data suggested that Wnt/ß-catenin pathway might be a potential target to treat the LPS-induced inflammation in ALI.
Palabras clave
Texto completo:
1
Banco de datos:
MEDLINE
Asunto principal:
Beta Catenina
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Lesión Pulmonar Aguda
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Células Th17
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Vía de Señalización Wnt
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Pulmón
Límite:
Animals
Idioma:
En
Revista:
Biochem Biophys Res Commun
Año:
2018
Tipo del documento:
Article
País de afiliación:
China