In the case of bacterial infection and mucosal injury neutrophil transepithelial migration is essential for host defense and tissue homeostasis, however, it may also lead to detrimental inflammation, which is a hallmark of inflammatory disorders of mucosal surfaces, particularly diseases of the gastrointestinal tract, including ulcerative colitis and Cohn’s disease. Our laboratory focuses on interactions of innate immune cells, specifically neutrophils with luminally expressed epithelial adhesive receptors, and the contribution of these interactions to regulation of epithelial barrier and mucosal wound healing, under the conditions of intestinal inflammation. A better understanding of the mechanisms regulating PMN recruitment and retention at the mucosal surfaces, and identification of specific molecules that may link PMN-epithelial cell interactions with epithelial barrier function and wound repair are imperative for the development of new and improved therapeutic approaches aiding in the resolution of mucosal inflammation, and reestablishing epithelial homeostasis. Reaserch Interest: • Understanding mechanisms regulating leukocyte recruitment to mucosal tissues • Determining the underlying mechanisms for leukocyte-associated effects on endothelial/epithelial function • Host-pathogen interactions • Innate immune contribution to colorectal cancer