74 Antibiotic Treatment Suppresses Rotavirus Infection and Enhances RV-Specific Immunity

Abstract

ALDH2-/mice showed a drastically low intake of ethanol-containing diet. Therefore, studies were continued using WT and ALDH2+/mice. In WT mice, ethanol increased inulin flux in distal colon (DC), but not in proximal colon (PC) or ileum. In ALDH2+/mice, not only inulin flux was high in DC, but also flux in PC, ileum and jejunum was increased by ethanol. High permeability was associated with the redistribution of TJ and AJ proteins from the junctions of DC in WT mice, and jejunum, ileum, PC and DC in ALDH2+/mice. LPS in liver was high in ethanol-fed ALDH2+/mice compared to that in ethanol-fed WT mice. Plasma ALT/AST, histopathology and fat-accumulation was also greater in ALDH+/mice. Ethanol-fed ALDH+/mice showed significantly higher level of acetaldehyde in colonic mucosa compared to that in WT mice. In Caco-2 cell monoalyers (lacks ADH), acetaldehyde, but not ethanol, disrupts TJs and AJs and increases inulin flux. Expression of ADH1B resulted in increased sensitivity to ethanol-induced TJ and AJ disruption. On the other hand, over expression of ALDH2 reduced sensitivity to acetaldehyde-induced TJ and AJ disruption. Conclusion: Our study demonstrates that ALDH2 deficiency increases sensitivity to ethanolinduced gut and liver injury.