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The epithelial sodium channel (ENaC) can increase the colonic absorptive capacity for salt and water. <i>Campylobacter concisus</i> is a common pathogenic epsilonproteobacterium, causing enteritis and diarrhea. It can induce barrier dysfunction in the intestine, but its influence on intestinal transport function is still unknown. Therefore, our study aimed to characterize <i>C. concisus</i> effects on ENaC using the HT-29/B6-GR/MR (epithelial cell line HT-29/B6 transfected with glucocorticoid and mineralocorticoid receptors) cell model and mouse colon. In Ussing chambers, <i>C. concisus</i> infection inhibited ENaC-dependent Na⁺ transport as indicated by a reduction in amiloride-sensitive short circuit current (&#8722;55%, <i>n</i> = 15, <i>p</i> &lt; 0.001). This occurred via down-regulation of &#946;- and &#947;-ENaC mRNA expression and ENaC ubiquitination due to extracellular signal-regulated kinase (ERK)1/2 activation, predicted by Ingenuity Pathway Analysis (IPA). In parallel, <i>C. concisus</i> reduced the expression of the sealing tight junction (TJ) protein claudin-8 and induced claudin-8 redistribution off the TJ domain of the enterocytes, which facilitates the back leakage of Na⁺ ions into the intestinal lumen. In conclusion, <i>C. concisus</i> caused ENaC dysfunction via interleukin-32-regulated ERK1/2, as well as claudin-8-dependent barrier dysfunction&#8212;both of which contribute to Na⁺ malabsorption and diarrhea.