Dietary pectin remodels commensal bacterial surfaces to promote IgA-mediated protection from intestinal inflammation.

Diet-microbe interactions shape mucosal immunity, yet how dietary cues drive strain-specific immunoglobulin A (IgA) responses remains poorly understood. Here, we show that dietary pectin induces a microbiota-dependent high-IgA phenotype in gnotobiotic mice mono-colonized with Bacteroides uniformis (B. uniformis). This effect is mediated by a pectin-responsive rcsC-associated regulatory program that remodels the bacterial surface. Comparative lipidomics identifies the glycosphingolipid HexCer (34:0) as a dominant feature of the remodeled bacterial surface. HexCer is recognized by the C-type lectin receptor CLEC4E on intestinal neutrophils, and CLEC4E deficiency abrogates IgA induction. Downstream of CLEC4E, neutrophil-derived APRIL (a proliferation-inducing ligand) promotes IgA class switching and enhances IgA coating of bacteria in vivo. This IgA response increases the mucosal association of B. uniformis and confers protection against colitis. Together, these findings uncover a diet-responsive bacterial program that generates an immunogenic glycosphingolipid signal to engage innate sensing and shape the mucosal IgA repertoire, thereby reinforcing mutualistic colonization.