Dr. Andrew Sawaya Receives HSF Translational Research Award

The Miller School of Medicine researcher is investigating the role of inflammation in wound healing.

Dr. Andrew Sawaya

University of Miami Miller School of Medicine research assistant professor of dermatology and cutaneous surgery Andrew Sawaya, Ph.D, recently received a Hidradenitis Suppurativa Foundation (HSF) grant awarded to scientists who conduct significant translational research on the chronic, inflammatory skin condition.

We sat down with Dr. Sawaya to discuss his work.

What inspired you to pursue a career in research?

When I was in undergrad, I was able to volunteer in a lab at the University of Miami in the biophysics department. I took a summer off and spent time in the lab and really liked it. I decided that was for me. So I continued, pursuing a master’s a degree at Johns Hopkins in biochemistry. That’s actually where I first got into skin biology. I was studying keratin proteins and their role in different diseases, like basal cell carcinoma.

When I finished I decided to come back to Miami. I started in Marjana’s (Marjana Tomic-Canic, Ph.D.) lab as a technician and decided to do my Ph.D. under her mentorship. I went to grad school here at UM and I stayed with Marjana. That’s how I got into wound healing research. I then did my post-doc at the NIH and investigated wound healing from a different perspective, looking at the oral mucosa. The oral mucosa actually heals a lot faster and more efficiently than cutaneous skin. The idea is to see why, to compare and contrast rapid wound healing to chronic, non-healing wounds. That’s how I got started.

Can you explain the key findings of your research on chronic wound healing and inflammation?

The longstanding thought in the field was there’s this inflammatory response in chronic wounds. We always thought it was hyperinflammation. Therapies would target inflammation, which explains why a lot of therapies targeting inflammation didn’t work for chronic wounds.

With oral mucosal and cutaneous skin wound healing, there’s this optimal inflammatory response that peaks and then is able to be resolved. But in chronic wounds, there’s suboptimal inflammation. It lingers and does more damage.

We found certain transcription factors involved with this process. We found certain inflammatory cells like neutrophils involved with processes like NETosis, increased NETosis, and its regulation, and how there’s increased NETosis in diabetic foot ulcers and different pathways involved with that. Our research is showing that there’s a suboptimal inflammatory response in these patients with chronic wounds.

How do you go from there to the next step of addressing a suboptimal inflammation response? This presents a counterintuitive shift, given the longstanding belief in the field regarding hyperinflammation in chronic wounds.

Exactly. Usually, all these skin diseases are highly inflammatory. You have to try to find a way to stimulate that inflammatory response, but not every inflammatory pathway is beneficial. So you have a specific type of inflammatory response.

And localized?

Exactly. There’s a lack of the mean cell recruitment to the site of the wound. I used this to stimulate proper inflammatory response, which is actually the beginning of the healing process. You have to have proper inflammation for the rest of the process of healing to proceed. It’s stuck in that early phase. And if you can target that early phase, you can put them on a proper projection.

What are your current research focuses?

I’m still pursuing wound healing research and tissue regeneration, but I’ve switched focus for the time being to other inflammatory diseases like hidradenitis suppurativa. It’s very interesting and there are a lot of things that go hand-in-hand with wound healing and HS.

You were recently awarded the HSF Translational Research Grant.

Yes, that’s in the works, as well as an aging project with The Miami Project that goes back to the idea of a suppressed inflammatory response in chronic wounds. With aging, chronic wounds tend to occur more frequently. (We’re investigating if) lack of inflammation due to a lack of inflammasomes contributes to chronic wounds that occur more frequently in the aging population.

Another aspect of my lab does is the impact of epigenetics on the infusion process to establish inflammatory memory.

You collaborate with different specialties. How do you think you can optimize those types of collaborations to yield the best results?

I think collaboration is necessary and very beneficial for everyone. I would strongly recommend trying to find as many collaborations as possible. You can share resources. Everyone has different expertise, so you can bring together different expertise from different backgrounds and different research techniques, as well. Collaborating is one of the most important things you can do.

What are you most excited for to see happening in the next five or 10 years in your research or in the field in general?

More therapies. If you look at chronic wounds, a lot of therapies have been tested and failed. There are only a handful of therapies approved by the FDA and they all show a limited efficacy. There’s a whole population of patients who don’t respond. I think that is a good area to pursue—why those patients fail to respond.

But also, what makes a chronic wound eventually heal. Some patients heal and some don’t. I think a good future direction is to try to understand why.

What advice do you have for aspiring researchers?

Network. Get to know people. Meet people in different fields who can help with your research. And you have to find something you really enjoy doing. Find something you really like doing and people who are more senior than you to give you good advice. We’ve been there and can act as mentors for you.

Tags: dermatology, Dermatology and Cutaneous Surgery, Dr. Andrew Sawaya, wound healing