Abstract

G A A b st ra ct s in inflamed colons compared to WT + 2% DSS mice suggesting greater degree of vasculogenesis under inflammatory conditions. Conclusion: These results show that lymphatic dysregulation through genetic ablation of FOXC2 significantly exacerbates the onset, progression and severity of experimental IBD. These data suggest that alterations in lymphatic patterning and valve formation (under FOXC2 control) may contribute to IBD progression. Although abnormal lymphatic patterning is not clearly linked with IBD development, therapies which preserve postnatal valve integrity may help to resist gut injury or recover gut integrity in IBD associated gut injury. With lymphatics playing such an important potential role in the pathophysiology of IBD, research focusing on factors interfering with lymphatic damage and therapy to restore lymphatic functioning may open new doors for treatment modalities targeting this area. This work supported by Department of Defense Grant ‘Lymphatic Vascular Based Therapy in IBD' (W81XWH-11-1-0577)

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