PP257 - EFFECTS OF VITAMIN D SUPPLEMENTATION ON GUT–LUNG AXIS INFLAMMATION IN MICE WITH DSS-INDUCED COLITIS
PP257
EFFECTS OF VITAMIN D SUPPLEMENTATION ON GUT–LUNG AXIS INFLAMMATION IN MICE WITH DSS-INDUCED COLITIS
Y.-P. Hao1,*, H.-Y. Fan1, C. L. Yeh1
1School of Nutrition and Health Sciences, College of Nutrition, Taipei Medical University, Taipei, Taiwan, Province of China
Rationale: Inflammatory bowel disease (IBD) is a chronic disorder that may also affect extraintestinal organs, including the lungs. Intestinal inflammation may affect lung immunity through the gut–lung axis. Vitamin D has immunomodulatory and barrier-protective properties, but its role in regulating gut–lung inflammation remains unclear. We aimed to investigate the effects of vitamin D supplementation doses on intestinal and lung inflammatory responses in mice with colitis.
Methods: Fifty-one male C57BL/6 mice were fed with diets containing 100, 1000, or 10000 IU/kg vitamin D3 for 5 weeks, followed by 2.5% DSS to induce colitis. Disease activity index (DAI), plasma 25(OH)D concentration, inflammatory cytokines in peritoneal lavage fluid, and mRNA expression of cytokines and tight junction proteins in mesenteric lymph nodes, colon, and lung tissues were analyzed.
Results: Compared with the low-dose vitamin D supplementation (LDS) group, mice in the high-dose vitamin D supplementation (HDS) group showed significantly lower DAI and colon injury scores. Although plasma 25(OH)D levels decreased after DSS treatment, they remained significantly higher in the HDS group. In peritoneal lavage fluid, levels of IL-1β, IL-6, and MCP-1 were lower in the HDS group. In the colon, ZO-1 expression was higher, whereas IL-17 expression was significantly lower in the HDS group than in the LDS group. In the lung, the HDS group exhibited decreased IL-1 expression, increased ZO-1 expression, and elevated IL-17 and IL-23 expression, suggesting that vitamin D may improve inflammatory status by regulating the gut–lung axis.
Conclusion: High-dose vitamin D supplementation may ameliorate DSS-induced colitis and may regulate the IL-23/IL-17 pathway to reduce distal pulmonary inflammation and maintain mucosal barrier integrity.
Disclosure of Interest: None declared