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Alcohol accumulation promotes esophagitis via pyroptosis activation

Gastroesophageal reflux impairs the mucosal barrier in the distal esophagus, allowing chronic exposure of the squamous epithelium to multitudinous stimulations and inducing chronic inflammation. Esophagitis is a response to inflammation of the esophageal squamous mucosa. Our study clarified that alc...

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Detalles Bibliográficos
Autores principales: Wang, Fengjiao, Li, Gang, Ning, Jinfeng, Chen, Lantao, Xu, Hai, Kong, Xianglong, Bu, Jianlong, Zhao, Weiwei, Li, Zhengtian, Wang, Xiuyun, Li, Xiaoguang, Ma, Jianqun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Ivyspring International Publisher 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6097477/
https://www.ncbi.nlm.nih.gov/pubmed/30123073
http://dx.doi.org/10.7150/ijbs.24347
Descripción
Sumario:Gastroesophageal reflux impairs the mucosal barrier in the distal esophagus, allowing chronic exposure of the squamous epithelium to multitudinous stimulations and inducing chronic inflammation. Esophagitis is a response to inflammation of the esophageal squamous mucosa. Our study clarified that alcohol accumulation could aggravate the progress of esophagitis by inducing pyroptosis; however, Ac-YVAD-CMK, an inhibitor of caspase-1, could effectively suppress the expression of IL-1β and IL-18 both in vivo and in vitro, reducing the inflammatory response, which is promised to be an agent to inhibit the progression of esophagitis. Additionally, caspase-1-derived pyroptosis is involved in esophageal cancer.