The Role the Th17 Response in Nitrogen Dioxide-promoted Allergic Airway Disease
After graduating from George Mason University in 2004 and taking two years off from school, I entered UVM’s (former) MD/PhD program. I am currently a seventh year MD/PhD student in the fifth year of my PhD training in the Cell and Molecular Biology program. Since November of 2009, I have been working under the guidance of Matthew Poynter. A member of the Vermont Lung Center, the Poynter laboratory studies lung inflammation and asthma. And just as importantly, our laboratory offers camaraderie and Matt is an exceptional mentor. When I am not hypothesizing, writing, reading, and experimenting, you can find me somewhere in the wilderness: rock climbing, mountain biking, hiking, or skiing. Find me if you’d like to learn some interesting lung immunology or need a belay.
Our laboratory’s primary research focus is on the innate and adaptive immune responses that develop following exposure to environmental pollutants, as well as inflammatory chemicals produced by the lung. In humans, these inflammatory events are believed to manifest as clinical asthma.
The environmental pollutant nitrogen dioxide (NO2) is a byproduct of combustion and a component of car exhaust. NO2 exposure is correlated with asthma development and severity. In our animal model of NO2-promoted allergic airway disease, the immune response that develops following NO2 exposure (in the presence of the antigen ovalbumin, i.e. egg white protein) is reminiscent of that observed in severe asthma. While severe asthma comprises only 5-7% of the asthmatic population, severe asthma represents 40-50% of asthma health care costs and is resistant to current standards of treatment. Becca’s project is focused on the characterization, functional relevance, upstream requirements for and potential therapeutic interventions of the Th17 response in NO2-promoted allergic airway disease.
Ather, J.L., Ckless, K., Martin, R., Foley, K.L., Suratt, B.T., Boyson, J.E., Fitzgerald, K.A., Flavell, R.A., Eisenbarth, S.C., and M.E. Poynter. Serum amyloid A (SAA) activates the NLRP3 inflammasome and promotes TH17 allergic asthma in mice. Journal of Immunology, 2011, 187(1):64-73, PMC3119761.
Ckless, K., Hodgkins, S.R., Ather, J.L., Martin, R., and M.E. Poynter. Epithelial, dendritic, and CD4+ T cell regulation of and by reactive oxygen and nitrogen species in allergic sensitization. Biochemica et Biophysica Acta – General Subjects 2011, 1810(11):1025-34, PMC3140554.
Martin, R.A., Ather, J.L., Lundblad, L.K.A., Suratt, B.T. Boyson, J.E., Budd, R.C., Alcorn, J.F., Flavell, R.A., Eisenbarth, S.C., and M.E. Poynter. Interleukin-1 Receptor and Caspase-1 are Required for the Th17 Response in NO2-Promoted Allergic Airway Disease. Submitted for publication to the American Journal of Respiratory and Cell and Molecular Biology Dec 2012.
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