Fig. 8

Inflammasome activation by acute alcohol binge in the small intestine is attenuated by in vivo inhibition of ER stress. a Activation of inflammasome components caspase-1 and IL-18, including the active cleaved forms Casp-1 p10 and IL-18 p18, were assessed by Western blot and quantified (b) from the PSI of pair-fed (PF), chronic alcohol without binge, 10 day EtOH 4 h binge and 10 day EtOH 9 h binge mice. c ER stress inhibition through in vivo 4-phenylbutiric acid (4-PBA) administration was used to reduce CHOP expression and inflammasome target IL-18 activation was measured by Western blot and quantified (d) from PF and 10 day EtOH 9 h binge mice. e Western blot analysis and quantification (f) of cleaved (clv) PARP from PF and alcohol-fed mice with and without 4-PBA treatment. g Activation of IL-18 was measured by Western blot and quantified (h) in the PSI of PF and 10 day EtOH 9 h binge mice, as well as EtOH mice treated with anti-IL-17 antibody or an isotype control. n = 5–7 mice/group; p < 0.05 * vs. pair-fed, # vs. 10 d EtOH No binge, † vs. 10 day EtOH 4 h binge, ° vs. 10 day EtOH 9 h binge