The tight junctions (TJ) connecting the adjoining intestinal epithelial cells form a barrier that deny luminal antigens an access to host tissue, and prevent excessive immune response and inflammation. Patients with inflammatory bowel disease (IBD) have a leaky gut, characterized by an increase in intestinal TJ permeability.
We study mechanisms of 
TJ barrier dysfunction and explore ways of enhancing the TJ barrier to prevent intestinal inflammation. Currently we are investigating how autophagy, a selective degradation pathway, enhances intestinal TJ barrier by targeting pore forming TJ proteins to lysosomal degradation and selectively sort TJ barrier forming proteins out of constitutive degradation pathway.
We also study transcriptional regulation of TJs by Aryl Hydrocarbon Receptor (AhR) Pathway and have developed a novel AhR agonist that may offer a natural, non-toxic therapeutic tool against IBD.
Macrophage elastase MMP-12-induced degradation of basement membrane and macrophage migration through TJs is another area under investigation.
Go Guts!
Follow us: @NighotPLab
Gut Research Interest Group
Pubmed Link
The lab is looking for a committed graduate student. Write to pnighot@pennstatehealth.psu.edu.
Latest:
Congratulations, Ashwin, on this new manuscript!
- Another benefit of autophagy- Our new paper shows that autophagy is not just a degradation pathway. Congratulations, Kushal, for this publication.
- New manuscript
- American Journal of Physiology-Cell Physiology@AJPCellPhys
