Imagine that you're in the prime of your age, that you have no energy because you're constantly

confronted with having to deal with explosive diarrhea, that you have to confront with

wearing a diaper to work, and you have to always think twice before taking a step out

in the open, in the wild, having to think whether there is a toilet where you can do

your business.

Unfortunately such is the life for several of our patients who suffer from inflammatory

bowel disease.

And it's not few lives that we are talking about.

There are approximately three million persons in Europe alone that are affected, and this

translates to approximately five billion dollars per year in terms of healthcare costs that

we have to face.

And the disease is characterized by inflammation of the gut, and this inflammation can happen

in different parts of the gut, allowing the doctors to diagnose Crohn's disease from ulcerative

colitis.

Now, this devastating disease is what brought me to Erlangen, because we have an excellence

cluster here in Erlangen that investigates this disease.

And as a young PhD student diagnosed with Croctitis myself, I was wondering what could

it be that led to this kind of a situation.

So in our guts we have a single monolayer of epithelial cells that distinguish the self

from the non-self, the bacteria, and the environment.

And this is the situation that you would very frequently encounter in a patient if you look

at the gut.

This is the normal situation, and here you have a ulcer.

You have a break in this epithelial barrier.

The cells are gone.

All these immune cells are now in contact with the environment.

And that obviously means a lot of trouble.

As soon as these immune cells encounter the bacteria and the environment, they trigger

epithelial cell death.

And to give you an analogy of this, these are epithelial cells.

They are healthy, like Harry and Hermione and Ron.

And these are the stem cells sitting at the bottom of the crypts, happily producing more

new epithelial cells.

But then, in IBD patients, an unknown factor, the one that we cannot name, suddenly appears

and leads to the death of the stem cells of the gut.

Now this is a big problem because this means that you will not be able to create new epithelial

cells, and that is one of the cause and one of the consequences of the disease.

I was not very satisfied with this picture.

And I always ask myself, where are the good guys?

Like where are they?

Where are they hiding?

So to figure this out, I was in search for the molecule that is self-healing.

The body must produce a molecule that can limit this kind of cell death of the epithelium.

And when we took a deeper dive in the patient data sets, we figured out that one very interesting

pathway, which is arachidonic acid metabolism, seems to be lost in these patients.

They don't seem to produce much of this particular molecule.

Now if you look at arachidonic acid, it's a target for several common drugs.

I'm sure you all have taken painkillers, diclofenacibuprofen, and so on.

And these can block the production of prostaglandins.

And these are the molecules which I postulated to have this protective effect.