Michael C. Seeds, Ph.D.

Assistant Professor, Internal Medicine-Molecular Medicine; Pulmonary, Critical Care, Allergy and Immunologic Diseases

Email: mseeds@wfubmc.edu

Education:

Wake Forest University, Department of Internal Medicine, Section on Infectious Diseases, fellowship, 1987-1988

Wake Forest University, Department of Biochemistry, Ph.D., 1987

University of Virginia, Department of Biology, M.S. 1981

University of Virginia, Department of Biology, B.A.  1976

Research Interests:

The regulation of granulocyte secretory phospholipases A₂ and their contribution to inflammation and host defense.

Current Research:

Projects in my laboratory seek to understand how otherwise normal innate immune functions of granulocytes contribute to tissue injury and inflammation in the context of lung diseases, such as ARDS and asthma.  The current focus is the regulation and activation of secretory phospholipase A₂ enzymes that hydrolyze phospholipid membranes in and on target cells. Relevant membrane systems include: 1) hydrolysis of surfactant phospholipids during lung injury, 2) hydrolysis of bacterial membranes during antimicrobial host defense, 3) hydrolysis of eukaryotic cell membranes to release eicosanoid inflammatory mediators, and 4) hydrolysis of eukaryotic cell membranes to stimulate or resolve apoptosis. My research approaches are to delineate inflammatory biochemistry from lung tissues ex vivo, and model putative mechanisms regulating sPLA₂ using cell line models and recombinant proteins, in vitro.  These laboratory studies utilize a variety of techniques, including molecular biology, microscopy, biochemistry, and cell physiology to understand the function and regulation of these enzymes.  Collaborations include investigations of surfactant injury during asthma, granulocyte apoptosis, innate immunity, and genetic variations in sPLA₂ genes which impact on pulmonary diseases.  The goal of this work is to identify those granulocyte/innate immune functions that can be therapeutically abrogated during inflammation from those that should not.

Recent Publications:

Weaver KL, Ivester P, Seeds MC, Case LD, Arm J, Chilton FH. Effect of dietary fatty acids on inflammatory gene expression in health humans. J Biol Chem. 2009 Apr 9;284:15400-15407.

Seeds MC, Peachman KK, Bowton DL, Sivertson, KL, Chilton FH. Regulation of Arachidonate Remodeling Enzymes Impacts Eosinophil Survival During Allergic Asthma. Am J Respir Cell Mol Biol. 2009 Jan 16

Hite, RD, Seeds MC, Grier BL, Possmayer F, Veldhuizen RA, Waite, BM. Regulation of Hydrolysis by Secretory Phospholipases A2 in Surfactant Monolayer Films. Am J Respir Crit Care Med. 2009 April;179:A6278.

Sivertson KL, Seeds MC, Long DL, Peachman KK, Bass DA. The differential effect of dexamethasone on granulocyte apoptosis involves stabilization of Mcl-1L in neutrophils but not in eosinophils. Cell Immunol. 2007 Jun 13.

El Mezayen R, El Gazzar M, Seeds MC, McCall CE, Dreskin SC, Nicolls MR. Endogenous signals released from necrotic cells augment inflammatory responses to bacterial endotoxin. Immunol Lett. 2007 Jul 31;111(1):36-44. Epub 2007 May 25.

Hite RD, Seeds MC, Jacinto RB, Grier BL, Waite BM, Bass DA. Lysophospholipid and fatty acid inhibition of pulmonary surfactant: non-enzymatic models of phospholipase A2 surfactant hydrolysis. Biochim Biophys Acta. 2005 Dec 30;1720(1-2):14-21.

Pascual RM, Carr EM, Seeds MC, Guo M, Panettieri RA Jr, Peters SP, Penn RB. Regulatory features of interleukin-1beta-mediated prostaglandin E2 synthesis in airway smooth muscle. Am J Physiol Lung Cell Mol Physiol. 2006 Mar;290(3):L501-8.

Hite RD, Seeds MC, Safta AM, Jacinto RB, Gyves JI, Bass DA, Waite BM. Lysophospholipid generation and phosphatidylglycerol depletion in phospholipase A(2)-mediated surfactant dysfunction. Am J Physiol Lung Cell Mol Physiol. 2005 Apr;288(4):L618-24.

Publications:
For a listing of additional publications, refer to PubMed, a service provided by the National Library of Medicine