Lab Members

The intersection between chronic inflammatory skin diseases (such as atopic dermatitis and psoriasis) and the underlying immune environment during times of stimulation (such as vaccination) and disease (both viral and bacterial pathogens).

My focus is collecting clinical samples/metrics to better understand the relationship between S. aureus and bullous pemphigoid. Specifically, I am interested in whether this bacterium contributes to the molecular and/or phenotypic characteristics of disease severity. To do this I am enrolling patients to quantify S. aureus burden as well as examine biomarkers within serum and blister fluid to establish a role of this bacterium in disease pathogenesis.

Identifying the contributions of the mycobiome to skin in health and disease.

My research focuses on investigating how S. sureus proteases contribute to the development of bullous pemphigoid (BP) pathogenesis. Using biospecimens collected from BP subjects, I am isolating S. aureus strains to quantify protease gene expression. Furthermore, I am examining the role of the S. aureus protease glutamyl endopeptidase V8 (sspA) to identify whether this specific protein contributes to BP180 cleavage (through genetically manipulating the bacteria). This work will advance our understanding of BP disease mechanisms that drive blister formation and autoimmune responses and ultimately identify microbial-derived products as clinically relevant targets for intervention in BP.

My project aims to identify the effect of eczema-associated fungi on regulating skin inflammation and barrier function. Specifically, I study how fungal species (such as Candida albicans and Candida parapsilosis) influence protease activity on the skin and  initiate pro-inflammatory cytokine responses.

I am investigating the role of Staphylococcus aureus in the development of bullous pemphigoid (BP), an autoimmune blistering skin disease. My research focuses on whether S. aureus presence is associated with various metrics of BP disease severity and whether isolates from individuals with more severe disease preferentially influence the expression and cleavage of BP180, the protein associated with blister formation. To do this I am analyzing bacterial abundance from skin swabs acquired from subjects recruited at URMC. The goal of this study is to identify bacterial species that contribute to BP disease pathogenesis.