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. Author manuscript; available in PMC: 2019 Nov 19.
Published in final edited form as: Mucosal Immunol. 2019 May 19;12(4):930–944. doi: 10.1038/s41385-019-0170-4

Figure 10. Increased IL-17 production, Paneth cell activation, inflammasome and ER stress in the proximal small intestine after acute-on-chronic alcohol in mice.

Figure 10.

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. Supplementary Table 1