Data Sheet 1_MiR-29a deficiency disrupts gut microbiota-bile acid homeostasis and impairs the anti-inflammatory effects of lithocholic acid in colitis.pdf

While microRNA-29a (miR-29a) is a recognized epigenetic regulator of intestinal inflammation, its role in shaping microbiota-driven bile acid metabolism, particularly secondary bile acid production, remains unclear. This study aimed to investigate how miR-29a regulates microbiota-bile acid axis, with an emphasis on lithocholic acid (LCA) and its anti-inflammatory effects in colitis.</p>Methods<p>Colitis was induced in wild-type and Mir29a/Mir29b-1 locus-deficient mice using dextran sulfate sodium (DSS), and disease severity, colonic injury, and inflammatory responses were assessed.

Fecal microbiota composition and bile acid profiles were characterized using 16S rRNA gene sequencing and targeted metabolomics. Alterations in bile acids were further examined in relation to disease severity. In vitro, Caco-2 cells were used to evaluate the anti-inflammatory effects of LCA under modulation of miR-29a expression.</p>Results<p>MiR-29a/b1 deficiency significantly exacerbated DSS-induced disease severity, colonic injury, inflammatory responses, and epithelial ultrastructural damage.