Meet the Researcher - Allyson Molzahn
MEET THE RESEARCHER LIVE ON APRIL 28
Breakout Room: 23
Researcher Name: Allyson Molzahn
Title of Research: SARS-CoV-2 and Asthma - A key inflammatory cytokine may reduce susceptibility to COVID-19 infection
Division Representing: Health Sciences
Institution: University of Arizona
Institution Location: Arizona
Home State: Arizona
District Number: 3
Advisor/Mentor: Monica Kraft, Dave Francisco
Funding Source: NIH
My first undergraduate research experience was an internship at Barrow Neurological Institute with the Romanovsky Fever Lab studying thermoregulation. In addition to running experiments, I processed and analyzed data and assisted during surgeries. After this initial experience, I sought out research opportunities at the University of Arizona, which led me to my current lab, the Kraft Asthma Lab. In this role, I have studied cell culture, helped to develop a new project with recombinant DNA, and utilized various techniques for measuring protein expression. Outside of research, I pursued diverse volunteer experiences. During the first year of undergraduate, I volunteered as a tutor at Banner University Medical Center where I supported continuity with schoolwork for pediatric patients. I also began volunteering as a simulation assistant at the Arizona Simulation Technology and Education Center (ASTEC), a training resource for the University of Arizona College of Medicine Tucson (COM-T). As an ASTEC volunteer, I conducted health care simulations, directed tours and orientations, and helped prepare interdisciplinary trainings for health care professionals. I expanded my experience with COM-T as a Pre-MD Ambassador where I assist the Admissions Office in facilitating and proctoring interviews. After volunteering in this position for a year, I entered a leadership role as president. This expanded my duties to include planning professional development workshops and philanthropy events. Currently, I am volunteering as a COVID-19 contact tracer for the Maricopa County Department of Public Health to aid in the collection of critical public health data regarding the spread of SARS-CoV-2.
As a member of the Honors College at the University of Arizona, I was offered the opportunity to complete an independent study project in the first year of my undergraduate studies. I chose to study overall satisfaction of visitors and patients at Banner University of Medical Center and how it changes throughout the day. Under the guidance of a supervising physician, I collected basic survey data, which I analyzed and synthesized into a poster presentation. During the summer of 2018, I worked as a research intern at Barrow Neurological Institute with the Romanovsky Fever Lab studying thermoregulation. After carrying out various experiments, I processed and analyzed the collected data in order to present them at a poster presentation symposium. As the only student presenting on thermoregulation, I received various follow-up questions to my presentation and its relationship to other disciplines.
Significance of Research:
Several chronic lung-based co-morbidities show increased severity and mortality associated with SARS-CoV-2 infection - a notable exception being asthma. A key SARS-CoV-2 receptor, Angiotensin-converting enzyme 2 (ACE2), is highly expressed in nasal epithelium, making the upper airway a concern for SARS-CoV-2 entry. We aimed to determine any differences in ACE2 expression in nasal epithelial cells from asthmatic participants compared to normal participants. Gene expression dataset, GSE19187, contained nasal epithelium data from children with allergic diseases.. ACE2 expression was compared among disease status and its association with type 2 asthma biomarkers were investigated. Separately, we cultured primary human nasal epithelial cells from adult asthmatic and atopic healthy participants. Cells were treated with IL-13, a key inflammatory cytokine mediator of asthma, and ACE2 protein assessed using ELISA. GSE19187 analysis showed lower ACE2 expression in participants with allergies, asthma, and higher type 2 asthma signatures. Additionally, we identified negative correlations between ACE2 expression and three type 2 asthma biomarkers: IL-13, Periostin, and CLCA1. Protein analysis from cultured cells revealed IL-13 treatment significantly decreased ACE2 expression in asthmatic and atopic normal nasal epithelium. The gene expression data GSE19187 from children's nasal epithelium demonstrated reduced ACE2 expression in allergic participants depending on disease severity. A significant reduction in ACE2 expression resulted after IL-13 treatment in both asthma and atopic normal samples. Upcoming ACE2 RT-PCR experiments will complement these studies. These data suggest endogenous cytokines associated with asthma and/or allergic phenotypes may decrease ACE2 expression, potentially reducing susceptibility to SARS-CoV-2 infection.
Uniqueness of Research:
The COVID-19 pandemic has fundamentally changed our world, country, community and families. The type 2 cytokines associated with asthma and/or allergies are associated with a decrease in ACE2, a critical SARS-CoV-2 entry factor. These data demonstrate that individuals with type 2 phenotypes may have reduced susceptibility to SARS-CoV-2 infection, differing from other lung-based co-morbidities.
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