Background/Objective: Probiotic and vitamin D supplements are widely studied in clinical and animal studies as potential treatments for inflammatory bowel disease. However, their potential synergistic or additive effect in ameliorating colitis development is still poorly understood. The aim of this study was to investigate the potential beneficial enhancement of combining a mixed-strain probiotic with vitamin D supplementation in a colitis animal model. Method: After 5 days of acclimation, C57BL/6 mice received Vivomixx probiotic (at least 1 × 10⁹ Colony-Forming Units) and/or vitamin D (5 IU/g) in drinking water and chow, respectively, for 7 days prior to intracolonic TNBS-induced colitis and until sacrifice. On day 10, animals were sacrificed, and colons were collected to assess colonic damage, cytokine and chemokine expression, total M1 macrophage phenotype, and neutrophil recruitment. Serum and fecal samples were collected to assess vitamin D levels and microbiome composition. Results: Administration of probiotic and vitamin D alone or combined decreased colonic damage and neutrophil recruitment and activity. This effect was associated with an increase in the active form of vitamin D in serum and mucosal barrier integrity. However, administration of probiotics and/or vitamin D did not modulate macrophage infiltration or the M1 pro-inflammatory phenotype. Conclusions: These results suggest that combined probiotic and vitamin D supplementation attenuates TNBS-induced colitis by targeting neutrophil infiltration while enhancing the mucosal barrier. This alternative approach may offer protective potential for IBD management.

Introduction: Voluntary physical activity reduces lesion development and inflammatory parameters in experimental endometriosis, though the mechanisms remain unclear. Peroxisome proliferator-activated receptor γ (PPAR-γ), a regulator of inflammation and nociception, may mediate these effects. We previously observed PPAR-γ overexpression in lesions of endometriosis animals and hypothesized that it underlies exercise-induced benefits. Methods: Adult female Sprague-Dawley rats were randomized to three groups ( n = 12/group): endometriosis-vehicle, endometriosis-vehicle + exercise, or endometriosis + PPAR-γ antagonist + exercise. Endometriosis was induced by suturing four uterine horn fragments on the intestinal mesentery (day 0). Exercised animals had continuous access to a running wheel. Pain behaviors (Von Frey, hot plate) were assessed, and vesicles, blood, peritoneal fluid, and tissues were collected on day 61. Results: Exercised rats had higher food consumption ( p < 0.001) without differences in body weight at sacrifice, and a reduced fat-to-body weight ratio ( p < 0.0001). All groups showed higher pain sensitivity after surgery, unaffected by PPAR-γ antagonism. Exercise significantly reduced vesicle development and colonic damage compared to the non-exercised group, while these effects were abrogated by the PPAR-γ antagonist. Serum MIP3 alpha levels increased in exercised rats (p<0.05), with no significant differences in other cytokines. Conclusion: Our results indicate that PPAR-γ signaling contributes to the beneficial effects of exercise on endometriotic lesion growth.