Keio University

Elucidating the Therapeutic Mechanism of a Crude Drug for Inflammatory Bowel Disease: A First Step Toward Developing a Novel Treatment

Publish: May 18, 2022
Public Relations Office

May 18, 2022

Keio University School of Medicine

Ehime University

A research group from the Keio University School of Medicine, led by Professor Takanori Kanai of the Division of Gastroenterology and Hepatology, Department of Internal Medicine, Lecturer Tomohisa Sujino of the Endoscopy Center, and Project Assistant Professor Yusuke Yoshimatsu, in a joint study with Professor Takeshi Imamura and his colleagues from the Department of Molecular Pathophysiology, Ehime University Graduate School of Medicine, has demonstrated that the crude drug indigo naturalis, known to be effective in suppressing inflammation in patients with ulcerative colitis, induces immunosuppressive immune cells (regulatory T cells; Tregs) directly beneath the colonic epithelium.

Ulcerative colitis is a chronic inflammatory bowel disease of unknown cause, with many cases being difficult to treat. A previous multi-center joint study, led by the same department, demonstrated the efficacy of indigo naturalis for ulcerative colitis, and it has already been reported that components of indigo naturalis may be involved in the regeneration of the intestinal epithelium. The current study has shown that in both mice and patients with ulcerative colitis, indigo naturalis induces a population of Tregs with a unique gene expression profile directly beneath the epithelium, mediated through the colonic epithelium.

Further development of this research to elucidate the mechanism by which these Tregs repair the epithelium could lead to a novel therapeutic approach, distinct from conventional treatments for ulcerative colitis that primarily focus on suppressing the immune system.

The results of this research were published in the international multidisciplinary academic journal "Cell Reports" on May 10, 2022, at 11:00 a.m. (US Eastern Time).

Please see below for the full press release.

Press Release (PDF)