1989-1991: University of Minnesota, Duluth, MN
1991-1993: Montana State University, Bozeman, MT. Department of Microbiology - B.S. with honors in Microbiology
1993-1998: University of Utah, Salt Lake City, UT. Department of Pathology, Division of Cell Biology and Immunology - Ph.D. in Experimental Pathology
1998-2002: University of Vermont, Burlington, VT. Department of Pathology - Postdoctoral Fellowship
The influences of pulmonary innate and adaptive immunity on respiratory health and disease.
The research focus of the Poynter lab is to investigate the crosstalk between the airway epithelium and resident or inflammatory leukocytes in the initiation and modulation of innate and adaptive immune responses. In particular, the lab focuses on the genesis of allergic asthma, attempting to determine how environmental components can cause the development of an allergic response against an otherwise innocuous inhaled antigen. The understanding gained into the initiation of allergy is also used in the lab to develop and test novel therapeutic approaches in preclinical models. For instance, the Poynter lab identified Serum Amyloid A (SAA) as an endogenous mediator of allergen sensitization that promotes mixed Th2/Th17 allergic responses, exacerbates pre-existing allergic airway disease, and operates through the TLR2/Nlrp3-dependent generation of IL-1ß. Responsiveness to IL-1ß is required for the Th17 response and may, therefore, be a therapeutic target for severe asthma.
Severe asthma is also manifest in obese subjects, and we are seeking to understand the contribution of adipose-derived factors to the activities of leukocytes and epithelial cells in obese allergic asthma. To this end, we are conducting clinical and pre-clinical studies examining the salutary effects of weight loss and accompanying alterations in these adipose-derived factors on airway epithelial activities and lung function. Specifically, we are examining the impact of altered airway epithelial mitochondrial activities on allergen-induced cytokine production and methacholine responses.
Current projects in the laboratory are exploring surgical and dietary modification of obesity-associated inherent and allergic asthma, as well as the function of adipocyte-derived extracellular vesicles, especially exosomes, on airway epithelial function. If you are inherently curious, have a passion for scientific inquiry, and have an applicable knowledge base and skillset, I welcome you to inquire about opportunities for working with our group.
Professor of Medicine
Director of Cellular, Molecular, and Biomedical Sciences doctoral program
Associate Director of the Vermont Lung Center
2012-2017 "Serum Amyloid A3 in Allergic Asthma: An Endogenous Mediator of Disease Severity", NIH/NHLBI R01 (Poynter)
2016-2021 "Obese Allergic Asthma and the Impact of Weight Loss on Airway Epithelial Function", NIH/NHLBI R01 (Poynter & Dixon)Ather JL, Foley K, Suratt BT, Boyson JE, and ME Poynter. Airway epithelial NF-kB activation promotes the ability to overcome inhalation antigen tolerance. Clinical and Experimental Allergy. 45(7):1245-1258 (2015) PMC4472492
Kien CL, Bunn JY, Fukagawa NK, Anathy V, Matthews DE, Crain KI, Ebenstein DB, Tarleton EK, Pratley RE, and ME Poynter. Lipodomic evidence that lowering the typical dietary palmitate to oleate ratio in humans decreases the leukocyte production of pro-inflammatory cytokines and muscle expression of redox-sensitive genes. Journal of Nutritional Biochemistry, S0955-2863(15)00178-3 (2015) PMC4679618
Ather JL, Chung M, Hoyt LR, Randall MJ, Georgsdottir A, Daphtary NA, Aliyeva MI, Suratt BT, Bates JHT, Irvin CG, Russell SR, Forgione P, Dixon AE, and ME Poynter. Weight loss decreases inherent and allergic methacholine hyper-responsiveness in mouse models of diet-induced obese asthma. American Journal of Respiratory Cell and Molecular Biology, 55(2):176-187 PMID 27064658 (PMCID in process)Hoyt LR, Ather JL, Randall MJ, DePuccio DP, Landry CC, Wewers MD, Gavrilin MA, and ME Poynter. Ethanol and other short-chain alcohols inhibit NLRP3 inflammasome activation through protein tyrosine phosphatase stimulation. In press Journal of Immunology, June 13, 2016 PMID 27421477 (PMCID in process)
Ather JL, Burgess EJ, Mandal MK, Matthews DE, Boyson JE, and ME Poynter. Uricase inhibits nitrogen dioxide-promoted allergic sensitization to inhaled ovalbumin independent of uric acid catabolism. Journal of Immunology, 197(5):1720-1732. PMID 27465529 (PMCID in process)
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