My research interest is in understanding the molecular mechanism of bacterial-epithelial crosstalk as it relates to the pathogenesis of intestinal inflammation in colitis and necrotizing enterocolitis (NEC), a life-threatening inflammatory bowel disorder of unknown cause that afflicts premature infants.
I have discovered that the components of the Toll-like receptor (TLR) pathway are partly responsible for bacteria-mediated changes in fucosylation of the gut epithelium, which plays a key role in epithelial barrier function in both immature and mature mice colon. TLR4-mediated cell signaling in the pathogenesis of NEC has attracted increasing attention in the NEC research field. The location of the receptor in the small intestine influences its function. However, the distribution of TLR4 in the developing human colon is totally unknown.
My current research focuses on the distribution and trafficking of TLR4 on developing human colon, and how TLR4 regulates the glycosylation of human fetal colon as it relates to NEC. The hypothesis is that the mechanisms by which LPS triggers TLR4 signaling in the immature colon may have a different phenotype compared to mature colon. This study may bring a new understanding to the genesis of NEC and may lead to the discovery of novel, TLR4-specific therapies for the prevention of NEC.