University of Vermont

College of Medicine

Vermont Center for Immunobiology and Infectious Diseases

Bio for Matthew Poynter, Ph.D.
Matthew Poynter, Ph.D.

Matthew Poynter, Ph.D.

Associate Professor of Medicine
Pulmonary Medicine
Department of Medicine


Contact Information
E-mail: matthew.poynter@uvm.edu
Office Location:
Medicine, Given Building, Room E410A

Education

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

Research Interests

Airway epithelial regulation of pulmonary innate and adaptive immunity.
The research focus of the Poynter lab is to investigate the crosstalk between the airway epithelium and antigen-presenting cells (macrophages and dendritic cells) 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 model environmental compound studied, nitrogen dioxide (NO2), is an oxidant gas that can be generated endogenously during infection or exogenously as a product of combustion processes. Furthermore, epidemiologic evidence indicates that individuals exposed to elevated levels of NO2 have an increased likelihood of developing asthma as well as having more severe disease. The understanding gained into the initiation of allergy is also used in the lab to develop and test novel therapeutic approaches in preclinical models. The Poynter lab has recently 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. Current projects in the laboratory are exploring the contribution of SAA3 to allergic sensitizations, asthma exacerbations, and pulmonary infectious disease.

Academic Appointments

2002-2003: Research Assistant Professor, Department of Medicine, University of Vermont
2003-2009: Assistant Professor, Department of Medicine, University of Vermont
2009 - present: Associate Professor, Department of Medicine, University of Vermont
2011 - present: Associate Director, Vermont Lung Center, University of Vermont

Research Grants

2012-2017 "Serum Amyloid A3 in Allergic Asthma: An Endogenous Mediator of Disease Severity", NIH/NHLBI R01 (Poynter)

2012-2015 "Airway Epithelial Control of Asthma Severity", Flight Attendant Medical Research Institute, Clinical Innovator Award (Poynter)

Publications

Ather JL, Alcorn JF, Brown AL, Guala AS, Suratt BT, Janssen-Heininger YMW, and ME Poynter. Distinct functions of airway epithelial NF-kB activity regulate nitrogen dioxide-induced acute lung injury. American Journal of Respiratory Cell and Molecular Biology, 43(4): 443-451, 2009.

Hodgkins SR, Ather JA, Paveglio SA, Allard JL, Whittaker-Leclair LA, Suratt BT, Boyson JE and ME Poynter. NO2  inhalation induces maturation of pulmonary CD11c+ cells that promote antigen-specific CD4+ T cell polarization in the lung. Respiratory Research, 11: 102, 2010.

Paveglio SA, Allard J, Foster SR, Ather J, Bevelander M, Mayette J, Whittaker LA, McCarthy SM,  van der Vliet A, Suratt BT, Boyson JE, and ME Poynter. Airway epithelial indoleamine 2, 3-dioxygenase inhibits CD4+ T cells dure Aspergillus fumigatus antigen exposure. American Journal of Respiratory Cell and Molecular Biology, 44(1): 11-23, 2011.

Ather JL, Hodgkins SR, Janssen-Heininger YMW, and ME Poynter. Airway epithelial NF-kB activation promotes allergic sensitization to an innocuous inhaled antigen. American Journal of Respiratory Cell and Molecular Biology, 44(5): 631-638, 2011
Ather JL, Ckless K, Martin R, Foley KL, Suratt BT, Boyson JE, Fitzgerald KA, Flavell RA, Eisenbarth SC, and ME Poynter. Serum amyloid A (SAA) activates the NLRP3 inflammazome and promotes TH17 allergic asthma in mice. Journal of Immunobiology, 187(1): 64-73, 2011.