Dr. Prashant Nighot's research has been focused on intestinal mucosal homeostasis in health and disease. The lab is interested especially in the role of defective intestinal tight junction (TJ) barrier in inflammatory bowel disease (IBD), including Crohn’s Disease and ulcerative colitis. TJ barrier defects allows penetration of luminal antigens leading to excessive immune and inflammatory response.

Recent work has focused on the role of autophagy in TJ barrier regulation. Autophagy, a cell survival mechanism, degrades unnecessary, misfolded and long-lived proteins and organelles and helps cell survive under stress. The lab's pioneering studies have shown that autophagy enhances TJ barrier via degradation of pore forming TJ protein claudin-2. Currently, the lab is conducting an NIH-funded study investigating the molecular mechanisms of autophagy regulation of TJ barrier and if autophagy-mediated enhancement of TJ barrier can prevent intestinal inflammation.

Dr. Nighot’s lab is also interested in investigating targets to combat IBD. One such recent project studies the role of aryl hydrocarbon (AhR) pathway in TJ regulation. In a collaborative study, the laboratory is using a novel, non-toxic ligand to activate AhR pathway to attenuate intestinal inflammation via enhancement of TJ barrier. Other projects in the laboratory include investigating the role of matrix metalloproteinases in intestinal inflammation and an NIH-funded study of the role of chloride channel ClC-2 in mucosal TJ barrier homeostasis.

The Nighot lab's studies employ in vivo approaches including several mouse models of intestinal inflammation, in vitro cellular and molecular methods and advanced imaging techniques to examine their hypothesis.