Improving the Odds: Interrupting Inflammation May Prevent Debilitating Progression of EoE

Catherine Ptaschinski, Ph.D., seeks to understand how food allergy can sometimes trigger an inflammatory response in the esophagus, instead of typical responses like nausea and airway restriction. Over time, this inflammation causes fibrosis where the esophagus becomes stiff. This makes it difficult and painful to swallow, and food can get stuck, requiring an endoscopy. Here she answers six questions about her work.

Catherine Ptaschinski, Ph.D., works on a microscope with a fellow researcher
Catherine Ptaschinski, Ph.D., right, is a researcher at the Mary H. Weiser Food Allergy Center.

What areas of food allergy are you currently investigating?

I am focused on the food allergy process of eosinophilic esophagitis (EoE), which is caused by infiltration of immune cells into the esophagus where they aren’t normally found and this leads to inflammation in the tissue. We are trying to figure out what these early inflammatory events are that lead to these later complications of the disease.

There’s a lot of overlap between allergy and gastroenterology in this. Patients are usually treated for heartburn first and if the heartburn treatment is not effective, then they are biopsied to see if they have EoE. It is a fairly recent development that we have recognized this overlap in symptoms.

Twenty or 30 years ago, there’s no way we would catch the disease this early. But now clinicians are becoming more aware of the prevalence of disease. If their patients are not responding to treatment, they will do a biopsy for EoE and confirm disease that way. It’s usually still at the earlier stages of the disease at this point.

I work both with clinical allergists and gastroenterologists — it depends on how a person’s disease manifests and what a person’s preferences are in terms of whether they would rather have a gastroenterologist or an allergist help manage their disease.

Why is this area of research important to the field of food allergy and how is it making a difference?

EoE has really only been recognized as a separate disorder in the last 30 years or so, so not much research has been done on this disease, and not very much is known about it.

Patients have really had to live with some debilitating symptoms and symptoms that have affected their quality of life for a long time. We are just now beginning to understand what the causes of this are and how we might be able to treat it.

What results have you found so far?

We’re looking at a specific inflammatory molecule called Stem Cell Factor that can activate multiple types of immune cells that are implicated in this disease. A lot of studies that have been done in the past have been looking at these molecules that target one type of cell or another, but we know that there are multiple cell types that can help drive this inflammation and drive the progression of disease.

We have found this one specific molecule that can activate many of the cell types that are important in driving this inflammation. We hope that that will provide a more general and broader treatment than treatments that others are looking at.

What is the significance of these results?

With this disease, typically in the earlier stages when there is just inflammation. That’s when things can be managed.

Once it gets to the later stage with the fibrosis, the stiff inflexible esophagus, there’s really nothing that can be done at this point. We’re interested in whether we can intervene early after diagnosis with this inflammation and if we can block that inflammation, we can therefore prevent these further complications.

“I think it’s important for people to understand that there is probably not just one answer to this disease.”

Catherine Ptaschinski, Ph.D.

What direction do you see your research taking in the future?

The next step is to move this into human tissue. We do know that the inflammatory molecules that we’re working on are increased in human disease. In terms of trying to block those pathways, currently everything is done in animal models. It’s still going to be a while, but our next big goal is whether we can translate this into humans.

Current treatments out there don’t work for everyone. One common treatment is food elimination, or just avoiding the food that triggers inflammation. But as many patients are unable to identify which food causes symptoms, food elimination doesn’t work for everyone.

The other commonly used treatment is long-term steroid use, but this has very significant side effects. There are a lot of patients that don’t respond to either one of those treatments, so new treatments are really needed.

What do you wish people understood about your research?

Not just with my research, but research in general, I wish that people understood that it takes many, many years to move research from animal models into a human therapeutic. We’re looking at probably 10 to 15 years at the minimum.

I also think it’s important for people to understand that there is probably not just one answer to this disease. We are looking at one specific inflammatory molecule. We think it’s important because we know that it targets all of the different cells that are involved in the initiation of inflammation, but we don’t think that this is necessarily the whole answer. This is one of many targets that may work as a therapeutic.

Not everyone’s disease is exactly the same, and it’s going to take lots of different people working together targeting multiple pathways.