The goal of our lab is to use genetic approaches to dissect novel antimicrobial peptide (AMP) signaling in host-microbe interactions and inflammatory diseases.
Project 1: Defensin signaling in psoriasis
Defensin levels are very high in psoriatic lesions and are biomarkers for psoriasis. In healthy skin, these peptides serve as a defense mechanism to prevent skin infections. In psoriasis patients, however, the levels of defensins are abnormally high without any infections. We found that defensins are important pro-inflammatory factors in the development of psoriasis and cause psoriatic itch. The objective for this project is to figure out exactly which immune cells and sensory neurons respond to defensins, and to identify cell surface receptors for defensins as potential therapeutic targets for psoriasis.
Project 2: Microbe-host interaction between Staphylococcus aureus and the mammalian defensin system
S. aureus is the most common cause of skin infections. When the skin gets infected, keratinocytes rapidly release defensins in response to infections. We will combine transcriptomics analyses, in vivo imaging, and mammalian and bacterial genetics to reveal how S. aureus copes with defensins and defensin-regulated immunity.
Project 3: Antimicrobial peptides in urinary tract infections
Urinary tract infections (UTIs) are among the most common and most painful bacterial infections, yet microbe-host interactions in the bladder and urinary tracts are severely understudied. Defensins are theorized to be a key component of the bladder innate immune system, and our research using novel mouse genetic tools aims to reveal exactly how these AMPs interact with the urinary microbiome, immune cells, and sensory neurons. Our goal is to identify defensin receptors on every defensin-responsive cell type, and to understand how each cell type contributes to bladder immunity or pathology during UTIs.