Matthew Poynter

Biography

Prof Matthew Poynter received his Ph.D.University of Utah, Salt Lake City, UT. Department of Pathology, Division of Cell Biology and Immunology - Ph.D. in Experimental Pathology. Currently, he is working as Professor in university of vermont. He has successfully completed his Administrative responsibilities as Professor. His research has included 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.

Research Interest

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.