University of Southern Mississippi
We are asking one of the most important questions in infectious disease:
Why does the human immune system — designed to kill bacteria — fail against Mycobacterium tuberculosis?
Tuberculosis still kills over 1 million people every year. Existing drugs work, but treatment takes months. Drug resistance is growing. And Mtb keeps finding ways to survive inside the very cells meant to destroy it.
Our lab is on a mission to change that.
We found that Mycobacterium tuberculosis secretes a molecule called polyphosphate (polyP) — and uses it to send a signal to your immune cells that says: “Don’t kill me.”
This signal shuts down the immune cell’s ability to destroy bacteria — even bacteria that would normally be killed instantly. We work to understand this signal at the molecular level — and find ways to block it.
Our research uses primary human macrophages and THP-1 macrophage cell lines, live Mtb infection models, genetics, imaging, and pharmacology — all aimed at one goal: finding the Achilles’ heel of TB.

PolyP is made by bacteria using an enzyme called polyphosphate kinase (PPK). Humans do not have PPK. This makes PPK an attractive drug target — we can potentially block bacterial polyP production without directly harming the human host.
NIH SuRE-FIRST R16 | Mississippi INBRE | USM Start-up Funds