Matthew D. Woolard, Ph.D.

Associate Professor

Contact Information:

Email: mwoola@lsuhsc.edu
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: 

Lipid metabolic regulation of macrophage function that contributes to disease pathogenesis.

Macrophages are heterogeneous cells of the immune system that contribute to antibacterial activity, tissue homeostasis, resolving inflammation and wound healing. Carrying out these diverse roles requires functional plasticity. This also means this plasticity can be disrupted resulting in the contribution of macrophage activity to the pathogenesis of numerous diseases. Lipid metabolism and lipid mediated signaling are crucial to the regulation of macrophages function. The goal of my laboratory is to understand how lipid metabolic enzymes contribute to macrophage function during disease. We are pursuing two areas of investigation to achieve this goal:

1) We are elucidating how arachidonic acid metabolism by Francisella-infected macrophages inhibits pro-inflammatory responses while promoting anti-inflammatory responses. This knowledge will allow us to modulate macrophage function in ways that enhance their antibacterial activity to control bacterial infections without the need for antibiotic therapy.

2) We are investigating how lipid metabolism by macrophages during atherosclerosis contributes to their pro-inflammatory state. A better understanding of these processes will likely identify new molecular target for the development of therapies to treat CVD.

Representative Publications:
Brummett AM, Navratil AR, Bryan JD, Woolard MD. 2013. Janus kinase 3 activity is necessary for phosphorylation of cytosolic phospholipase A2 and prostaglandin E2 synthesis by macrophages infected with Francisella tularensis live vaccine strain. Infect. Immun. 82(3):970-82.

Navratil AR, Brummett AM, Bryan JD, Woolard MD. 2014. Francisella LVS induction of prostaglandin biosynthesis by infected macrophages requires specific host phospholipases and lipid phosphatases. Infect Immun. 82(8):3299-311.

Navratil AR, Vozenilek AE, Cardelli JA, Green JM, Thomas MJ, Sorci-Thomas MG, Orr AW, Woolard MD. 2015. Lipin-1 contributes to modified low-density lipoprotein-elicited macrophage pro-inflammatory responses. Atherosclerosis. 242(2):424-32.

All Publications: PubMed