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NIH awards $1.83 million to advance IBD research

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A researcher at the University of California, Riverside has received a four-year, $1.83 million grant from the NIH to determine how the loss of a protective barrier in the intestine impacts inflammatory bowel disease, according to a press release.

The T-cell protein tyrosine phosphatase (TCPTP) protects the intestinal epithelial barrier function; however, TCPTP activity is slow in some patients with IBD, which can compromise this function, per the release.

“These defects result in increased intestinal permeability – a major contributor to chronic inflammatory diseases of the intestine such as IBD,” Declan McCole, PhD, associate professor of biomedical sciences at University of California, Riverside, School of Medicine, said. “Although TCPTP mutations increase the risk of developing IBD, there are no therapeutic strategies aimed at correcting the consequences of these mutations.”

With the support of this NIH grant, McCole and colleagues aim to identify the association between barrier function in intestinal epithelial cells and reduced TCPTP activity, per the release. They will look for molecular signaling pathways that are changed by the loss of TCPTP using molecular biology approaches. Additionally, the researchers will try to fix intestinal barrier defects in TCPTP-deficient cells, and in cells with TCPTP mutations by interrupting the Janus kinase (JAK) signaling pathway. Currently, these inhibitors are being tested on IBD patients in clinical trials, according to the release.

“When TCPTP activity is compromised, errors occur in remodeling cell junctions – the structures that regulate barrier function,” McCole said. “The goal of the study is to discover the mechanisms by which loss of TCPTP activity in patients contributes to intestinal barrier defects in IBD. In addition, we hope to identify if strategies to inhibit JAK signaling may prove particularly effective in patients with TCPTP genetic mutations.”

Disclosures: This grant is supported by the NIH.