Student Research Week: How a Special Bacteria and Vitamin D Impact Immunity

While growing up Joseph Vaccaro ’21MS was told that the mind is a beautiful thing that should be used to improve the world.

It’s that parental mantra that helped him discover his path from Montrose, Pennsylvania, to College of Medicine Professor Saleh Naser’s laboratory at UCF. Naser studies the association of Mycobacterium avium subspecies paratuberculosis(MAP) with Crohn’s disease and Type I diabetes. Vaccaro is conducting research in his lab as part of his doctoral work in biomedical sciences. He will be presenting part of his investigation during the Student Scholar Symposium this week. The symposium is part of  Student Research Week, which is free, open to the public and ongoing in the Student Union this week.

The graduate student’s ultimate goal is to become a vaccine designer at a biotechnology company or the Centers for Disease Control and Prevention. He wouldn’t be the first Knight to do it. Darin Edwards ’97 ’10MS ’11PhD was part of the team that created Moderna’s COVID-19 vaccine. Vaccaro wants to do his part, too.

Vaccaro shares some of his research findings and why it’s important to conduct studies.

Why are you pursuing your major or field of study?

I’ve always been fascinated by the mechanisms of infection and immunity. UCF has given me the opportunity to take a closer look at the boundary between host and pathogen in this course of study.

What does your research examine and how does it impacts the community?

My research looks at the effects of a bacterium called Mycobacterium avium paratuberculosis, or MAP, on vitamin D signaling in immune cells. This research is important for patients infected with MAP, which includes people with rheumatoid arthritis and Crohn’s Disease. The results show that vitamin D supplements may be less effective for reducing inflammation in MAP-positive patients. Most people know that vitamin D is important for bone health, but it’s also a critical signal for parts of the immune system and a lack of active vitamin D in a type of cell called macrophages leads to increased inflammation and a weakened response to bacterial infection. The data shows that MAP can stop macrophages from processing vitamin D’s signal in the cell, which lets the bacterium survive longer and cause more damaging inflammation. My colleagues and I discovered that a protein called cathelicidin is responsible for translating the signal from vitamin D into reduced inflammation and pathogen destruction, and MAP survives better when cathelicidin is blocked or absent.

How did did you develop the idea for your research project?

My project is part of an ongoing effort in Dr. Saleh Naser’s laboratory to examine how persistent mycobacterial infection affects the immune system, especially in the context of chronic disease. Previous work has identified changes in nicotine signaling in MAP-positive Crohn’s patients and worsening rheumatoid arthritis symptoms during MAP infection. A fascinating paper in 2019 discovered that M. (mycobacterium) tuberculosis, which is related to MAP, can interfere with vitamin D signaling in macrophages. Dr. (Ahmad) Qasem, our postdoctoral scholar, reasoned that something similar might be happening during MAP infection.

What should people know about your research?

This research hinges on the fact that most vitamin D in the human body is inactive and freely circulates in the blood. The kidneys can activate a small amount of inactive vitamin D during conditions of low calcium, but this isn’t enough to stimulate the immune cells and it can’t be fixed with normal commercial supplements, which are inactive. However, since MAP is susceptible to certain commercial antibiotic cocktails, the problem of blocked vitamin D signaling may be fixable in MAP-positive patients, which is what we are aiming to help people with.

Why does research matter to you?

I was raised to believe that our minds are a gift, and that knowledge is a tool to make the world a better place. Every bit of knowledge we create about human health is one tiny step towards easing suffering and making someone else’s life safer and better. I will always be proud to be a part of that process.

Why did you choose UCF?

I chose UCF because I was impressed with the breadth of programs and variety of innovative research opportunities offered. It seemed like a place where anyone could find their niche. The location of the campus in sunny Orlando certainly didn’t hurt either.

What are some of your other interests?

I like to read and write short stories, as well as play tabletop games.