Research

Kurdowska, Anna K., Ph.D.

← BACK  



Contact: anna.kurdowska@uthct.edu

Education:

1986, Ph.D. Biochemistry, Jagiellonian Univ., Cracow, Poland
1980, M.S. Biochemistry, Jagiellonian Univ., Cracow, Poland

Research Interest:

Innate immunity and inflammatory response; Inflammatory response in the lung and other organs related to the acute lung injury / acute respiratory syndrome (ALI/ARDS), infection with influenza virus (flu), tuberculosis, and atherosclerosis. ALI/ARDS can be described as a complex clinical syndrome that results in significant impairment of lung function.

Current Projects:

  • Regulation of innate immunity in lung inflammation.
  • Neutrophils, endothelial, and epithelial cells in the lung - activation and apoptosis.
  • IgG receptors (FcgammaRs), TLR4, and other pro-inflammatory receptors - regulation and signaling.

Lay Summary:

One of the possible mechanisms underlying an inflammatory disease, such as ALI/ARDS, is excessive recruitment of white blood cells, neutrophils (PMNs) to lungs or other organs. PMNs, the most abundant white cells in circulation, play a central role in the defense system of the host. Typically, PMNs migrate to affected areas where they, for example, inactivate microorganisms. On the other hand, the excessive release of various pro-inflammatory mediators by PMNs may result in host tissue injury.

Research Overview:

Our laboratory studies mechanisms underlying regulation of pro-inflammatory activities of neutrophils. Most current work is aimed at using unique models of ALI/ARDS, including influenza virus induced ALI, to evaluate contribution of cross talk between neutrophils and endothelial cells to the pathogenesis of these conditions. In parallel efforts, potential modulators of signaling pathways evoked by neutrophil - endothelial cross talk are being tested in several animal models (ALI/ARDS, influenza, and atherosclerosis) and in vitro systems. Understanding regulatory role that these pathways play during development of the inflammatory response will facilitate discovery of novel therapeutic agents.

Selected Papers and Abstracts:

NOTICE: Protected health information is subject to electronic disclosure.