ArticleJCI insight2025
Dietary salt intake worsens the Th17-dependent inflammatory profile of patients with cirrhosis.
Article in JCI insight, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
BACKGROUNDLiver cirrhosis is characterized by chronic inflammation and fibrosis, with Th17 cells playing a crucial role in its progression. Recent evidence suggests that dietary salt influences immune diseases by modulating Th17 differentiation. This study assessed the impact of dietary salt on Th17-driven inflammation in patients with compensated cirrhosis and explored its effects on liver injury in mouse models.METHODSA nondrug, open-label, nonrandomized study involved 37 patients with compensated cirrhosis, who were given personalized guidelines to reduce salt intake over 3 months. Changes in Th17-driven inflammation and liver function markers were assessed at baseline and after salt restriction. In parallel, the impact of a high-salt diet on hepatic CD4+ T cells was analyzed in mouse models of acute liver injury and fibrosis.RESULTSHigh salt intake was associated with Th17-mediated inflammation and correlated with markers of impaired liver function in these patients. Importantly, moderating salt intake through a personalized nutritional intervention was sufficient to reduce CD4+ T cell-mediated inflammation. Furthermore, analysis of RNA-seq data revealed enrichment of salt-induced Th17 gene signatures in both liver tissue and peripheral cells from patients with liver disease. Similarly, mice fed a high salt diet showed hepatic enrichment of Th17 cells and exacerbated liver fibrosis upon injury. Mechanistic studies revealed that high sodium conditions activated NF-κB and induced IL-6 production in hepatocytes, which may promote Th17 responses.CONCLUSIONDietary salt exacerbates Th17-driven inflammation and contributes to cirrhosis progression. Salt reduction may represent a viable therapeutic approach to manage inflammation in compensated cirrhosis.FUNDINGGrants PI19/01554 and PI22/01907 from Instituto de Salud Carlos III (Madrid, Spain), CDEI-03/20-A and CIPROM/2023/4 from Generalitat Valenciana (Valencia, Spain), CNS2023-145676 from the National Research Agency (AEI) (Madrid, Spain), and LCF/BQ/D121/11860047 from La Caixa Foundation (Barcelona, Spain).
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