Study Identifies Genetic Factors Involved with Early-onset Ulcerative Colitis
A research team with members at the University of California, Los Angeles (UCLA) has discovered genetic factors involved in a severe form of inflammatory bowel disease (IBS), pediatric ulcerative colitis.
A research team with members at the University of California, Los Angeles (UCLA) has discovered genetic factors involved in a severe form of inflammatory bowel disease (IBS), pediatric ulcerative colitis.
Prior studies revealed the effects of interleukin 10, a strong anti-inflammatory protein that cools down the inflammatory responses in the body, is weakened in patients with early-onset ulcerative colitis.
Eunok Im, PhD, the study’s first author and an assistant professor at Pusan National University’s School of Pharmacy, said, “We knew that interleukin 10 played a role. But recent clinical and experimental evidence indicated that in addition to this protein’s crippled action, there may be other genetic factors at work causing early onset of this disease.”
While IBS isn’t limited to a particular age group, research has found that the younger the patient, the higher the risk of developing colon cancer and liver damage, as the inflammation inherently constricts the connected bile ducts.
Im and other scientists from the David Geffe School of Medicine at UCLA and Pusan National University in South Korea found that phosphatase and tensin homologue (PTEN), a vital protein for cell functions including growth and communication, may work in tandem with interleukin 10 as a catalyst for the development of ulcerative colitis.These scientists created the first animal model identical to pediatric ulcerative colitis, specifically to aid in testing potential drug treatments.
The studies further suggested that even within mice without interleukin 10, lacking the PTEN gene triggered massive inflammation and fatal colon and colitis development at as early as one month after birth. This could also result in disrupted antibacterial activity spurring an alteration in the colon’s bacterial diversity. Observing the mice models, the research team found an immediate rise in Bacteroides that trigger extensive inflammatory diseases.
The mice models and related research findings can potentially set the stage for prevention as well as treatment methods for this currently incurable condition.
Another author of the study, Charalabos “Harry” Pothoulakis, PhD, noted, “Future study may help us better understand how this bacteria has the potential to elicit inflammation in the colon and explore the molecular mechanisms of how the bacteria impacts disease onset.”
