Matthew D. Woolard, PH.D.


Assistant Professor

Contact Information:
Email: Office Phone: 318-675-5763
Laboratory Phone: 318-675-4160
Office Fax: 318-675-5764

Education/Training:
Postdoctoral Study, University of North Carolina at Chapel Hill      
Ph.D., Biomedical Sciences, 2004, University of North Texas Health Science Center at Fort Worth

B.A., Biology, 1999, Austin College

Major Research Interests:  Francisella tularensis host-pathogen interaction with emphasis on immune evasion

Pathogenic bacteria and their hosts have had a two-way conversation for millions of years. This interaction has led to many measure/counter-measure responses by the host and bacteria. The host immune response has developed many mechanisms to neutralize and remove pathogen bacteria. In turn, pathogenic bacteria have developed mechanisms to alter and evade the host immune response.  F. tularensis clearly manipulates the host to alter immune responses.  The molecular mechanisms and consequences of host immune evasion by F. tularensis are poorly defined.  My laboratory is interested in defining these molecular mechanisms and interactions of immune evasion.  We are currently investigating the ability of F. tularensis to induce the production of prostaglandin E­2 (PGE2) from infected macrophages.  The induction of PGE2 inhibits T lymphocyte proliferation and the generation of strong pro-inflammatory Th1 T lymphocytes.  These alterations in cellular immunity impact the clearance of F. tularensis from the lungs of infected mice.  Experiments are in progress to identify the prokaryotic effector molecule and the eukaryotic sensor responsible for instructing the macrophage to make and secrete PGE2.  We are also investigating the impact of PGE2 production on the generation of T cell responses during respiratory tularemia.

Representative Publications:

Woolard MD, JE Wilson, LL Hensley, LA Jania, TH Kawula, JR Drake, JA Frelinger.  2007.
A. Francisella tularensis-infected macrophages release prostaglandin E2 that blocks T cell proliferation and promotes a Th2-like response
. J Immunol. 178:2065-74.

Hall JD, MD Woolard, BM Gunn, RR Craven, S Taft-Benz S, JA Frelinger, TH Kawula.  2008. Infected-host-cell repertoire and cellular response in the lung following inhalation of Francisella tularensis
Schu S4, LVS, or U112
. Infect Immun. 76:5843-52.


Woolard MD, JA Frelinger. 2008. Outsmarting the host:  bacteria modulating the immune response.  Immunol Res. 41:188-202.


Woolard MD, LL Hensley, TH Kawula, JA Frelinger.  2008. Respiratory Francisella tularensis live vaccine strain infection induces Th17 cells and prostaglandin E2, which inhibits generation of gamma interferon-positive T cells. Infect Immun. 76:2651-9. Epub 2008 Apr 7.

All Publications: PubMed