Paula Zamora, PhD
Assistant Professor, Genetic, Environmental and Inhalational Disease
Assistant Professor, Microbiology, Molecular Genetics and Immunology
pzamora@kumc.eduMore:
Professional Background
Dr. Paula Zamora is an Assistant Professor in the Division of Genetic, Environmental and Inhalation Disease within the Department of Internal Medicine at the University of Kansas Medical Center. Her research focuses on the interface between the mammalian host and respiratory pathogens, with expertise in cell biology, innate immunity, virology, and bacterial pathogenesis. The Zamora Lab investigates infections in the airways of individuals with cystic fibrosis—a genetic disease marked by chronic inflammation, recurrent infections, and progressive lung function decline. Dr. Zamora’s work aims to uncover how chronic airway inflammation disrupts immune responses and to identify therapeutic strategies that can reverse lung damage and improve outcomes for people with chronic airway diseases.
Research
Overview
The Zamora Lab seeks to uncover how chronic inflammatory cues reshape the epigenetic and metabolic landscape of the airway, and how these alterations modulate responses to bacterial and viral infections. Our work centers on the respiratory tract of people with cystic fibrosis (pwCF), a genetic disease characterized by persistent airway inflammation, chronic infections, and progressive loss of lung function. By dissecting how epithelial and immune cell responses are reprogrammed in this context, we aim to identify molecular mechanisms that drive host defense alterations. Ultimately, our goal is to inform the development of therapies that restore immune competence and improve respiratory function in chronic airway diseases.
How does repeated airway inflammation affect viral and bacterial infections?
pwCF experience chronic airway inflammation that alters immune responses and worsens susceptibility to respiratory pathogens. Our lab uses in vitro models of airway epithelium to study how repeated inflammatory stimulation reprograms epithelial and microbial behavior, particularly in response to viruses like RSV and rhinovirus and bacteria such as Pseudomonas aeruginosa. We aim to define the molecular mechanisms by which chronic inflammation contributes to disease progression and pathogen persistence.
What molecular changes underlie dysregulated immune responses in the CF lung?We investigate how chronic inflammation in the CF airway reshapes the epigenome, transcriptome, and metabolome, contributing to impaired host defense. While gene modifiers influence CF severity, they do not fully explain the variability in clinical outcomes. Our research maps chronic inflammation–induced molecular changes that distinguish long-term immune dysfunction from acute responses, with the goal of identifying pathways that drive disease progression.
Can the effects of chronic inflammation be reversed to preserve lung function in CF?
Epigenetic modifications are reversible and offer a promising avenue for therapy in CF, where inflammation-induced damage accumulates over time. Our lab explores the potential of targeted epigenetic interventions—including modulation of non-coding RNAs—to reprogram dysfunctional immune and repair pathways. These studies may lead to novel therapeutics that reduce pulmonary exacerbations, preserve lung function, and extend benefits to other chronic airway diseases such as asthma and COPD.