Ulcerative colitis is one of the most common forms of inflammatory bowel disease
and is characterised by inflammation of the colon and the rectum.
The walls of the colon — also known as the mucosa — become inflamed
and no longer provide an effective barrier between the inner cavity
and the surrounding connective tissue, allowing gut microbes to cross the epithelial layer.
This causes inflammation of the mucosa and leads to a raft of unpleasant symptoms
such as abdominal pain, diarrhea, fatigue and rectal bleeding.
There are several commonly used anti-inflammatory and immunosuppressive drugs,
but they come with side effects and aren't long-lasting for many patients.
Currently, 15% of people with ulcerative colitis will require surgery
to remove some or all of the colon within 20 years of diagnosis.
Luckily, new insights into the immunology of this condition
are helping scientists develop new effective treatments.
One new class of treatments is aimed at preventing the inflammation in the first place,
by bolstering the physical integrity of the colon's epithelium.
This keeps the immune-triggering bugs confined to the interior of the colon.
Some of these treatments work by exploiting a human protein called IL-22
which helps strengthen the epithelial layer.
One new drug in development targets the receptor for IL-22 on the epithelium itself,
activating it and thereby initiating healing of epithelial cells and the mucus layer.
This drug is currently in phase two trials.
Researchers are also trying to use a plant product called indigo naturalis
which encourages immune cells in the area to release IL-22, again healing the epithelial barrier.
There are also new therapies emerging that prevent immune cells from entering the affected area.
where they might become activated to invoke an inflammatory response.
One way to do this is to inhibit proteins called integrins which live on the surface of T cells.
A new antibody drug that works this way stops T cells from getting across the blood vessel wall
into the mucosa and also blocks their binding to the epithelium.
This drug appears to effectively reduce pain and inflammation.
Another group of drugs uses a totally different approach,
targeting key inflammatory signals between different immune cells.
For example, one new drug tampers with the cellular machinery inside T cells
so that they no longer respond to messages from macrophages.
In a pivotal phase three trial, this drug induced remission in over 40% of patients
and has now been approved for the treatment of active ulcerative colitis.
A final approach to treating this disease is to restore the healthy balance of the gut microbiome.
One way of doing this is to use probiotic bacteria streams.
Adding these commensal bacteria back into the intestine's gut community
has been shown to quell inflammation and restore normal intestinal function.
One particular probiotic, known as E. coli nissle, has been shown to keep symptoms at bay
just as effectively as widely used anti-inflammatory drugs.
Fecal transplantation from healthy donors is also being experimented with,
although results to date are conflicting.
At least one recent study on multi-donor stool transplantation has shown promising results however,
eliminating symptoms in a quarter of patients.
As new approaches to tackling this disease come onto the market,
the hope is that more patients will be free of symptoms for longer and won't go on to need aggressive surgery.