ArticleCell communication and signaling : CCS2026
MSCs-derived CRABP2 regulates Treg/CXCL1 to ameliorate alcohol-induced liver injury.
Article in Cell communication and signaling : CCS, 2026. 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
backgroundAlcoholic hepatitis (AH) is an inflammatory disease associated with high mortality. Mesenchymal stromal cells (MSCs) are promising immune regulators in modulating acute or chronic inflammation. However, the specific mechanism mediating the persistent inflammatory response during AH and therapeutic potential of MSCs remains unclear.
methodsWe performed MSCs infusion on an animal model of acute-on-chronic alcohol-induced liver injury. Inducible depletion of regulatory T cells (Treg) was achieved using Foxp3-DTR/EGFP transgenic mice. MSCs and anti-CXCL1 treatments were performed on Treg-depleted mice to further elucidate the mechanisms of Treg-mediated neutrophil infiltration.
resultsMSCs therapy ameliorated liver damage, and elevated the proportion of Treg by secreting cellular retinoic acid binding protein 2 (CRABP2). Treg deficiency exacerbated hepatic neutrophil infiltration upon alcohol stimulation, with elevated serum TNFα and the subsequent hepatocellular CXCL1 expression. Hepatic neutrophil infiltration in Treg-depleted mice cannot be reduced by MSCs or anti-CXCL1 treatment. Consistently, AH patients had decreased peripheral Treg proportion, with the activation of hepatic and peripheral CXCL1-neutrophil inflammatory axis.
conclusionsTreg are critical protective regulators during acute alcohol-induced liver injury. MSCs-derived CRABP2 increases Treg proportion to ameliorate alcohol-induced liver injury through regulating CXCL1/neutrophil axis, appearing as a promising strategy for limiting the persistent inflammatory response during severe AH.
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