Studying the Contribution of Skin Inflammation to Allergic Disease Progression

Our lab leverages advanced methodologies, including gene expression profiling, microbiome analysis, and immune cell characterization to study the genetic, microbial, and immune factors driving atopic dermatitis (AD) and its progression to asthma. We focus on microbial interactions, particularly with Staphylococcus aureus, and immune cell functions during inflammatory responses. By integrating these methods, we aim to identify biomarkers and therapeutic targets to improve early diagnosis and intervention in children with AD.

Lab Projects (2)

Elucidating the genetic contribution of an altered skin microbiome in AD

The skin microbiome plays a critical role in the development and progression of atopic dermatitis (AD). Alterations in microbial composition, particularly Staphylococcus aureus colonization, contribute to inflammation and disease exacerbation. Our lab investigates how S. aureus interacts with the host immune system, focusing on its gene expression alterations that impact disease severity. Through gene profiling and microbiome analysis, we aim to identify bacterial factors that drive skin inflammation and uncover potential therapeutic targets to prevent exacerbations and reduce the susceptibility of progression to other allergic conditions.

Distinguishing Immune Cell Functions that Drive Inflammation in AD

Immune cells play an important role in inflammatory responses during AD. Mast cells, specifically, are known to be critical drivers of allergic responses, but their role in AD is understudied. Our lab examines how mast cells interact with components of the skin, such as melanin, to influence their migration and degranulation. By studying these mechanisms, we aim to understand how mast cells contribute to skin inflammation and progression to allergic comorbidities. Our goal is to identify novel biomarkers that could inform early diagnosis of other allergic conditions thereby improving clinical outcomes for children with AD.