Scientists identify the cause of inflammatory bowel disease

Scientists, including one of Indian-origin, have discovered a mechanism by which healthy cells in the gut are compromised in patients with inflammatory bowel disease (IBD).

IBD produces inflammation that causes abdominal pain, bloating, and other symptoms, along with potentially serious long-term complications.

The team from the University of Texas, Southwestern Medical Center, found that Th17 cells -- essential for maintaining the integrity of the intestinal barrier and protecting against bacteria and viruses -- in patients with IBD become pathogenic.

In IBD patients, Th17 cells “create the inflammation that underlies the disease," said study leader Venuprasad Poojary, Associate Professor of Internal Medicine and Immunology at the varsity.

"Through our research, we now have a better understanding of the intracellular process that converts protective Th17 cells into disease-generating, pathogenic, inflammatory Th17 cells," Poojary added.

Further, while conducting the study on mice it was found that a lipid-interacting protein called Raftlin1 binds to receptor retinoic acid receptor-related-orphan-receptor-gamma t (ROR), a transcription factor in Th17 cells, as IBD develops.

Once in place, Raftlin1 attracts phospholipids in the body to combine with the ROR-gamma-t, eventually turning Th17 cells pathogenic that causes IBD.

"Identifying the role of Raftlin1 in facilitating the binding of phospholipids to ROR-gamma-t is a major step forward in our understanding of the diverse and opposing functions of Th17 cells," said Dr. Poojary.

"It's an important finding because Th17-targeting therapies have shown promising results with some autoimmune diseases. There is a great need for new pharmaceuticals that can effectively treat IBD, since about a third of patients with the disease don't respond to existing treatments. "These findings could serve as a platform for therapeutic strategies to control Th17-mediated inflammation in IBD and other diseases," Dr. Poojary said. (IANS)