Pinto bean supplementation prevents vascular dysfunction by modulating the gut microbiome in an interleukin-10-dependent manner in mice fed an atherogenic diet.

The risk of cardiovascular disease increases under gut inflammatory conditions, but the underlying mechanism remains unclear. Pinto bean (PB) consumption reportedly increases the ileal expression of the anti-inflammatory cytokine interleukin (IL)-10. We investigated the effects of PB supplementation on inflammatory signature and vascular endothelial function in mice. We hypothesize that the effect of PB is mainly mediated by IL-10. Eight-week-old female mice from a C57BL/6 J background were randomized to groups in a 2 × 3 design, with genotype (Il10+/+, WT or Il10-/-, KO) and diets (AIN-93 M [CON] diet, atherogenic diet with 36.5% fat kcal and 1% cholesterol [Ath], or Ath diet + 5% PB, wt/wt [Ath+PB]) as factors. Gut microbiota composition, fecal short-chain fatty acids (SCFAs), ileal T-cell populations, inflammatory markers, and vascular endothelial function were examined. In WT mice, PB supplementation preserved gut microbial diversity and maintained fecal butyrate concentrations compared with atherogenic diet alone (P< .05), while sustaining the relative abundance of SCFA-producing taxa (Alistipes, Roseburia). These microbial changes were accompanied by an increased proportion of ileal regulatory T cells (P < .001) and preserved acetylcholine-induced, endothelium-dependent vasodilation (P < .05). In contrast, IL-10 KO mice exhibited impaired endothelial function and reduced microbial diversity irrespective of diet, and PB supplementation did not significantly improve vascular or immune outcomes. Overall, PB supplementation was associated with preserved vascular endothelial function and favorable microbiota and immune profiles in WT but not IL-10-deficient mice, suggesting these dietary benefits require intact IL-10 signaling.