Education

Ph.D., Microbiology & Immunology, Louisiana State University Health Sciences Center – Shreveport (2010-15)

B.S., Chemistry, The University of Wisconsin – Green Bay (2006-10)

Research Interest

Macrophage internalization of oxidized low-density lipoprotein (oxLDL) within the arterial intima results in the formation of lipid-laden, pro-inflammatory foam cells that directly contribute atherosclerotic lesion initiation and growth. Pro-inflammatory macrophages remain an unexploited, but desirable target for the treatment of atherosclerosis. Reducing plaque intrinsic inflammation by targeting foam cells in addition to reducing cholesterol biosynthesis/deposition (statin therapy) could enhance outcomes for individuals with cardiovascular disease. However, the molecular basis of macrophage foam cell pro-inflammatory activity remains poorly understood.

I am currently applying UPLC/MS/MS-based lipidomics to gain a more detailed understanding of oxLDL-elicited changes in macrophage lipid composition and arachidonate metabolism.

Publications

Becker, F., et al., A Critical Role for Monocytes/Macrophages During Intestinal Inflammation -associated Lymphangiogenesis. Inflamm Bowel Dis, 2016. 22(6): p. 1326-45 . PMID: 26950310

Navratil, A.R., et al., Lipin-1 contributes to modified low-density lipoprotein-elicited macrophage pro-inflammatory responses. Atherosclerosis, 2015. 242(2): p. 424-32. PMID: 26288136

Navratil, A.R., et al., Francisella tularensis LVS induction of prostaglandin biosynthesis by infected macrophages requires specific host phospholipases and lipid phosphatases. Infect Immun, 2014. 82(8): p. 3299-311. PMID: 24866789

Brummett, A.M., et al., 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, 2014. 82(3): p. 970-82.PMID: 24343645

Webmaster: Dennis Office

Disclaimer

2017