The School of Veterinary Sciences in Bristol may appear an unlikely place for Crohn’s disease research to occur – but recently, ground-breaking results published by scientists there have indicated a cause for fibrosis that affects sufferers of this debilitating condition. The work could have implications for patient treatment, as the current options are limited in outcome.
Crohn’s disease is a multifactorial condition that may affect any part of the digestive tract, from oesophagus to large bowel. Inflammation and ulceration may lead to fibrosis – thickening and hardening of the gut walls. If this does occur, the digestive tube loses its distensible and motile properties, which severely impairs function. In fibrosis, proteins (e.g. collagens) produced in the normal healing process are brought into play rather more than required.
Interleukin-13 (IL-13) is the protein implicated by this study. Previous research has shown that this soluble cytokine mediates fibrosis in the lung, kidney and liver, so perhaps it is not surprising that the gut should also be affected. The research team compared aspects of normal intestine with those from Crohn’s patients. Tissue culture demonstrated that IL-13 lessened the necessary factors for undesired collagen deposition, as in other instances of fibrosis.
According to Dr Jenny Bailey, a researcher in the study, “We have identified a novel population of IL-13-producing cells which, in intestinal samples, were found at very high levels in fibrotic muscle. Understanding how fibrosis occurs will help us to develop new medicines to treat patients.” It is hoped that IL-13 may present as a drug target in treatments that could prevent fibrosis from occurring.
Currently, Crohn’s patients with fibrosis face surgical intervention – about 30% of patients will have fibrotic tissue excised from their gut. The downside to this is that a shorter gut is less functional, which compounds existing digestive problems and intra-abdominal pain.
