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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 8. Inflammasome activation by acute alcohol binge in the small intestine is attenuated by in vivo inhibition of ER stress.

Figure 8.

(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, 10d EtOH 4h binge and 10d EtOH 9h 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 10d EtOH 9h 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 10d EtOH 9h 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 10d EtOH No binge, † vs 10d EtOH 4h binge, ⁰ vs 10d EtOH 9h binge.