Monthly Archives: January 2018

Barrier function of colonic epithelium is compromised in IBD patients and contributes to colonic inflammation. Previously, we showed that aftiphilin (AFTPH) is significantly downregulated in colonic biopsies from UC patients and involved in receptor re… Continue reading →

While FOXP3+ regulatory T cell (Treg) dysfunction has been linked to human inflammatory bowel disease (IBD), molecular mechanisms for disease pathophysiology are unclear. The transcription factor FOXP3 via histone methyltransferase EZH2 suppresses infl… Continue reading →

Recently, genetic variants conferring risk for IBD were fine-mapped to single variant resolution. Eight of these causal variants resulted in amino acid substitutions while ten were non-coding. The mechanism by which these non-coding causal variants con… Continue reading →

Loss-of-function mutations in the protein tyrosine phosphatase non-receptor type 2 (PTPN2) gene locus increase IBD susceptibility. We reported that PTPN2 knockdown (PTPN2-KD) in intestinal epithelial cells (IECs): (i) increased IFN-g activation of STAT… Continue reading →

Practicing patient-centric care by incorporating patient preferences in IBD care is increasingly recognized to be important. However, existing IBD disease activity measures do not incorporate patient perspective. Here, we describe the development of a … Continue reading →

Distinguishing between inflamed Meckel’s diverticulum (MD) and ileal Crohn’s disease (CD) can be challenging. We present a case of suspected MD in a patient with CD. Continue reading →

Cystathionine-β-synthase (CBS) & cystathionine-γ-lyase (CSE), convert homocysteine into cysteine & produce H2S, an anti-inflammatory mediator. In rodent colitis models, CBS & CSE activity is elevated and inhibition or knockout of CSE worsens colitis & decreases levels of anti-inflammatory cytokine IL-10. IL-10 KO mice develop spontaneous colitis accompanied by homocysteinemia & decreased H2S production, which are reversed by IL-10 administration. However, the cellular source of CSE-dependent IL-10 production is unknown. Continue reading →

A20 (TNFAIP3) suppresses inflammation by interrupting the NF-kB pathway via its ubiquitin-editing activities. Several single-nucleotide polymorphisms (SNPs) have been shown to be associated with various autoimmune and inflammatory diseases, including IBD. Two such SNPs are rs146534657 (A305G) and rs2230926 (T380G) have minor allele frequencies of 0.1-1.3% and 6.1-17.9%, respectively. We investigate the frequencies of these SNPs in our majority (>60%) Hispanic population and explore their clinical impacts on IBD. Continue reading →

Twitter, a popular social networking service, enables users to interact with messages (tweets) limited to 140 characters. It is an increasingly powerful mechanism to convey information. There is limited data on the use of Twitter for disseminating medi… Continue reading →