THOUSANDS of people suffering from Crohn’s disease could be saved from crippling symptoms and repeated surgery, after researchers discovered a new treatment for the condition.
The condition, which is currently incurable, is caused by inflammation that blocks the intestines and affects around 115,000 people in the UK.
Symptoms include diarrhoea, severe abdominal pain and extreme tiredness and often leads to repeated surgery to remove blocked sections of the gut.
People with Crohn’s disease can go for long periods without experiencing symptoms or but the periods where symptoms flare up.
However, scientists believe that drugs already on the shelves could prevent the inflammation that leads to fibrosis – or tissue scarring – which causes the blockages.
Researchers infected mice with a type of salmonella that mimics the symptoms of Crohn’s.
They discovered a gene mutation that prevented some of the mice from developing fibrosis.
The mutation switched off a specific hormone receptor, which stimulated part of the body’s immune response. It is this inflammatory response, that researchers believe causes the fibrosis.
Professor Kelly McNagny, co-author from the University of British Columbia (UBC), Canada, said: “Fibrosis results from inflammatory cells stimulating cells to produce this matrix, or scarring.
“We found what we think are the inflammatory cells that drive fibrosis. The gene that was defective in those cells is a hormone receptor.”
He added: “We found a way of targeting those cells so that we can dampen them down and prevent fibrosis.”
The medication which could treat the problem could already be on the shelves, the scientists revealed.
Professor McNagny added: “There are drugs available that may be able to block that hormone receptor in normal cells and prevent fibrotic disease.”
The new findings could also pave the way for treating other types of fibrosis.
The research could help experts treat liver scarring, chronic kidney disease, scarring caused by heart attacks and damage caused by ageing.
Bernard Lo, a PhD candidate at UBC, and study author said: “Fibrosis is a response to chronic inflammation, but it is also a process that occurs during normal ageing.
“If you can reverse this, you’ve essentially found a way to promote regeneration rather than degeneration. If you get liver cirrhosis, your liver stops functioning because you replace that normal health liver with scar tissue.
“It is the same thing in cardiac muscle. If you have a heart attack, you replace normal heart muscle with scar.”
Further research will be carried out to test possible drugs on mice.
Professor McNagny added: “We think that we can potentially block complications of all these age-related fibrotic diseases by dampening these particular inflammatory cell types.”
The study was published in the journal Science Immunology.