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LRRK2 G2019S enhances immune response pathways and aggravates asthma in mouse models.
Yang, Kai; Zhou, Yaolong; Cui, Jie; Tang, Weifeng; Chen, Yujun; Chen, Xiqun.
Afiliación
  • Yang K; Department of Integrative Medicine, Huashan Hospital, Fudan University, Shanghai, China.
  • Zhou Y; Department of Integrative Medicine, Huashan Hospital, Fudan University, Shanghai, China.
  • Cui J; Department of Integrative Medicine, Huashan Hospital, Fudan University, Shanghai, China; Institute of Respiratory Diseases, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, China. Electronic address: cuij1998@163.com.
  • Tang W; Department of Integrative Medicine, Huashan Hospital, Fudan University, Shanghai, China.
  • Chen Y; Department of Integrative Medicine, Huashan Hospital, Fudan University, Shanghai, China.
  • Chen X; Department of Integrative Medicine, Huashan Hospital, Fudan University, Shanghai, China; Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA, USA. Electronic address: chen_xiqun@fudan.edu.cn.
Biochem Biophys Res Commun ; 734: 150593, 2024 Aug 31.
Article en En | MEDLINE | ID: mdl-39217812
ABSTRACT
Asthma is a complex inflammatory airway disease that arises from the interplay between genetic predisposition and environmental influences. Leucine-rich repeat kinase 2 (LRRK2), a gene commonly associated with Parkinson's disease, has recently gained attention for its role in immune regulation and inflammation beyond the brain. However, its involvement in asthma has not yet been reported. In this study, we used LRRK2 G2019S transgenic mice and LRRK2 knockout mice to establish asthmatic models to explore LRRK2 impact on asthma. We found that LRRK2 G2019S transgenic mice showed exacerbated airway hyperresponsiveness (AHR) and airway inflammation in asthma mouse models induced by house dust mite. RNA sequencing data unveiled that the LRRK2 G2019S mutation enhanced immune response pathways, including NOD-like receptor, cellular response to interferon ß and activation of innate immune response signaling. Conversely, LRRK2 deficiency attenuated AHR and airway inflammation in the same asthma models. Our study offers new insights into the role of LRRK2 in allergic inflammation and highlights its potential as a therapeutic target for asthma.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: Biochem Biophys Res Commun Año: 2024 Tipo del documento: Article País de afiliación: China Pais de publicación: Estados Unidos
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
Buscar en Google

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: Biochem Biophys Res Commun Año: 2024 Tipo del documento: Article País de afiliación: China Pais de publicación: Estados Unidos