Dr. Anna Kurdowska is currently a full professor but also serves as the Associate Vice President for Research Compliance / Research Compliance Officer, Director of Research, and Director of Vivarium. Dr. Kurdowska came to the University of Texas Health Science Center at Tyler as Research Associate Specialist in 1991 and joined the faculty in 1992. She received her post-doctoral training in the Department of Biochemistry at the University of Georgia, Athens, Georgia.

Dr. Kurdowska’s research focuses on cellular pathogenesis of severe inflammatory conditions, including exposure to environmental tobacco smoke or second-hand smoke, influenza infections, Streptococcal pneumonia, acute lung injury/acute respiratory distress syndrome (ALIARDS), and atherosclerosis. She has discovered that Bruton’s tyrosine kinase (Btk) is a master regulator of pro-inflammatory processes in the alveolar compartment and vasculature (PCT/US15/23267, US Patent Application 15129956 and US Patent 9982265; Inhibition of Bruton’s Tyrosine Kinase (Btk) in the Lung to Treat Severe Lung Inflammation and Lung Injury, 2018). Her lab team’s work has been aimed at using unique animal models, many of which has been developed by their group, to evaluate the contribution of pro-inflammatory cells to pathogenesis of inflammatory lung diseases and cardiovascular ailments. In parallel efforts, potential modulators of signaling pathways have been tested in these models. Further, Dr. Kurdowska’s team routinely performed cell specific interventions in vivo in the above described models.

Dr. Kurdowska has published over 69 articles and has trained many graduate students and postdoctoral fellows. She also serves on various institutional committees, and is an editor or reviewer for a number of peer reviewed journals and ad hoc reviewer for Federal funding agencies.

Education and Training

1988-1991: Postdoctoral Research Associate, Dept. of Biochemistry, Univ. of Georgia, Athens, GA
1981-1986: PhD, Biochemistry, Jagiellonian University, Cracow, Poland
1978-1980: MS, Molecular Biology / Biochemistry, Jagiellonian University, Cracow, Poland
1975-1978: Molecular Biology, Jagiellonian University, Cracow, Poland

Recent Academic and Administrative Appointments

2021 - : Radiation Safety Officer for Research
2021 - : Associate Vice President for Research Compliance, Univ. of Texas / Health Science Center, Tyler, TX
2019 - 2021: Associate Dean of School of Medical and Biological Sciences; responsible for research operations and compliance.
2019 (August to November) and 2021 - present: Authorized Signing Official for sponsored projects.
2017 - : Research Compliance Officer, Univ. of Texas, Health Science Center, Tyler;
Responsible for monitoring compliance related to research activities to assure that all Institutional, U.T. system, State and Federal policies are followed.
2012 - : Director of Research / Director of Vivarium, Univ. of Texas, Health Science Center, Tyler; Responsible for research operations and vivarium oversight.
2012 - 2013: Interim Chair, Department of Cellular and Molecular Biology (previously Dept. of Biochemistry), Univ. of Texas, Health Science Center, Tyler
2008 - : Professor of Biochemistry, Dept. of Biochemistry, Univ. of Texas, Health Science Center, Tyler

Courses Taught

BIOT 5132 - Critical Reading II Course
BIOT 5222 - Advanced Metabolism: Signal Transduction
BIOT 6334 - Advanced Immunology
BIOT 5310 - Fundamentals of Biomedical Research
BIOT6312 - Biotechnology II: Immunochemistry

Research Interest

• One of the possible mechanisms underlying an inflammatory disease, such as lung infection, 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.

• Other cells also play important role in pathogenesis of inflammatory disease. These include macrophages (tissue specific white blood cells called monocytes), endothelial and epithelial cells (cells building vascular walls).

• Activation and life span of inflammatory cells is highly regulated through receptors (proteins that respond to stimuli and govern functions of cells).

• Engagement of pro-inflammatory receptors triggers signaling cascades (sets of proteins that start, multiply and stop intracellular signals) that control cellular behavior.

• Dr. Kurdowska’ s group has been harnessing novel discoveries (based on types of research studies described above) to develop new therapeutic modalities for inflammatory diseases (translational approach).

Publication Highlights

1. Kurdowska AK, Florence JM. Promoting Neutrophil Apoptosis to Treat Acute Lung Injury. Am J Respir Crit Care Med. 2019 Aug 1;200(3):399-400.

2. Florence JM, Krupa A, Booshehri LM, Davis SA, Matthay MA, Kurdowska AK. Inhibiting Bruton's tyrosine kinase rescues mice from lethal influenza-induced acute lung injury. Am J Physiol Lung Cell Mol Physiol. 2018 Jul 1;315(1):L52-L58.

3. Florence JM, Krupa A, Booshehri LM, Gajewski AL, Kurdowska AK. Disrupting the Btk Pathway Suppresses COPD-Like Lung Alterations in Atherosclerosis Prone ApoE-/- Mice Following Regular Exposure to Cigarette Smoke. Int J Mol Sci. 2018 Jan 24;19(2).

4. Florence JM, Krupa A, Booshehri LM, Allen TC, Kurdowska AK. Metalloproteinase-9 contributes to endothelial dysfunction in atherosclerosis via protease activated receptor-1. PLoS One. 2017 Feb 6;12(2):e0171427.

5. Krupa A, Fol M, Rahman M, Stokes KY, Florence JM, Leskov IL, Khoretonenko MV, Matthay MA, Liu KD, Calfee CS, Tvinnereim A, Rosenfield GR, Kurdowska AK. Silencing Bruton's tyrosine kinase in alveolar neutrophils protects mice from LPS / immune complex induced acute lung injury. Am. J. Physiol. Lung Cell. Mol. Physiol. 307:L435-L448, 2014.

6. Krupa A, Fudala R, Florence JM, Tucker T, Allen TC, Standiford TJ, Luchowski R, Fol M, Rahman M, Gryczynski Z, Gryczynski I, Kurdowska AK. Bruton’s tyrosine kinase mediates cross-talk between FcγRIIa and TLR4 signaling cascades in human neutrophils. Am. J. Respir. Cell Mol. Biol., 48:240-249, 2013.