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TAINAN, Taiwan

Inflammatory bowel diseases (IBDs), which include Crohn’s disease and ulcerative colitis, are mysterious; however, a medical discovery made by joint effort between National Cheng Kung University (NCKU) in Taiwan and University of California in the USA, published in Nature, provides new insight into how inflammation triggers tissue repair and regeneration, as well as a healing pathway to treat IBDs.

Dr. Li-Wha Wu, a professor at the Institute of Molecular Medicine from College of Medicine at NCKU, worked with the researchers at Laboratory of Gene Regulation and Signal Transduction in University of California to conduct the study.

According to Wu, “Further therapeutic efforts in treating IBDs should aim at normalizing IL-6 expression rather than a complete blockage of the signaling, thereby restoring the balance of immune system and mucosal healing in these patients.”

IBDs are chronic relapsing diseases that lead to structural damage with destruction of the bowel wall, explained by Wu who added that the patients often suffer from chronic diarrhea, mal-absorption, weight loss, rectal bleeding, and abdominal pain, and many require surgery over time.

She also said, although IBDs are not common among Asians, their incidence rate is increasing in Taiwan due to the Westernized environment and life style.

Based on the National Health Insurance Research Database, the prevalence rate of ulcerative colitis had significantly increased by almost 10-fold from 0.72 in 1998 to 7.05 in 2008 for each 100,000 people.

Wu indicated that consistent with chronic inflammation being a major contributor to cancer growth and metastasis, long-standing IBD patients also has a higher tendency of developing colorectal cancer than those without the disease by 2-10 fold depending on the studies.

Wu noted, the elevation of the pro-inflammatory interleukin-6 (IL-6) family, leading to the activation of its co-receptor, glycoprotein 130 (gp130), is frequently detected in IBDs.

In the study, mice bearing an intestinal mucosa-specific active gp130 mutant were treated with dextran sulfate sodium to induce IBD-like diseases in mice for studying the role of IL6-related signaling through gp130 in IBDs.

The activation of gp130 signaling promoted intestinal mucosal regeneration through an unconventional activation of a key player involved in the control of organ sizes, Yes-associated protein (YAP).