Fig. 10 | Mucosal Immunology

Fig. 10

From: Alcohol-induced IL-17A production in Paneth cells amplifies endoplasmic reticulum stress, apoptosis, and inflammasome-IL-18 activation in the proximal small intestine in mice

Fig. 10

Increased IL-17 production, Paneth cell activation, inflammasome and ER stress in the proximal small intestine after acute-on-chronic alcohol in mice. Working model based on our data indicates that acute binge on chronic alcohol exposure results in increased abundance of Paneth cells in the PSI, leading to ER stress induction, IL-17A release, apoptosis and inflammasome activation in crypts in the PSI. The mechanistic role of alcohol-induced IL-17A is indicated by experiments where IL-17 blocking antibody prevented alcohol-induced ER stress, apoptosis, inflammasome activation and IL-18 production in isolated crypts in vitro and in vivo in the PSI

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