Nicholas W. Lukacs, Ph.D.
Associate Professor
Campus Address:
5214 MED Sci I 0602
1301 Catherine Road
Ann Arbor, Michigan 48109-0602
Phone: 734/936-1856
nlukacs@umich.edu
Annual Report | Biography | Research Interests | Selected Publications
Departmental Annual Report
Brief Biography
Dr. Lukacs received his Masters degree in 1988 from the University of New Hamshire and his Ph.D degree from Wayne State University in 1992 in the Department of Immunology/Microbiology. He then took Postdoctoral training in the Department of Pathology at the University of Michigan Medical School in the laboratory of Steven L. Kunkel, Ph.D., from 1992-1993 where he examined the role of chemokine and cytokine networks in immune/inflammatory responses.
Upon completion of his post-doctoral training he became a member of the Department of Pathology faculty at the University of Michigan as an Assistant Research Scientist. Dr. Lukacs has received NIH funding to examine the role of chemokines and cytokines in the allergic airway inflammatory response associated with asthma. His Departmental activities include teaching a graduate level class in the role of immune responses in disease progression.
Dr. Lukacs’s research interests involve the regulation of cytokine and chemokines during eosinophilic airway inflammation, the role of mast cells in chronic inflammation, and the role of stem cell factor (SCF) in acute and chronic inflammation.
Research Interests
Asthma and pulmonary viral infections, cytokines, chemokines, T lymphocyte regulation in pulmonary disease eosinophil biopsy.
Our laboratory has focused on the interrelationship
of cytokines, chemokines, and leukocyte activation during asthmatic-type
airway responses and immune responses. We have specifically identified
particular leukocyte populations that have an effect during different
stages of the allergic responses within the lung. The pathological manifestations
of an allergic airway response are a culmination of several coordinated
events involving the participation of multiple mechanisms of and cell
types. The early release of mast cell-derived arachadonic acid metabolites,
production of early response cytokines, increased expression of adhesion
molecules and production of chemokines, all lead to the recruitment of
multiple cell types with the ability to participate in the allergic airway
response. We have specifically identified mediators that are involved
at each of these steps in the activation pathway and utilize physiological
measurements of the lung to determine the relevance of each mediator in
disease progression. The coordinated use of animal models related to clinical
observations will allow the further elucidation of the mechanisms involved
in the initiation, maintenance, and regulation of allergic airway inflammation
leading to airway damage and help identify pharmaceutical targets.
Selected Publications
Hogaboam, C.M., Blease, K., Mehrad, B., Steinhauser, M.L.,
Standiford, T.J., Kunkel, S.L., and Lukacs, N.W. Chronic airway hyperreactivity,
goblet cell hyperplasia and peribronchial fibrosis during allergic airway
disease induced by A. fumigatus. Am J Pathol. 156:723-2000.
Oliveira, S.H.P., C.M. Hogaboam, and N.W. Lukacs. SCF-induced
airway hyperreactivity is dependent upon leukotriene production. Amer.
J. Physiol. - Lung 280(6):L1242-9, 2001.
Lukas, N.W., M.M. Glovsky, and P.A. Ward. Complement-dependent
immune complex-induced bronchial inflammation and hyperactivity. Am. J.
Physiol. - Lung 280:512-518, 2001.
Tekkanat, K.K., H.F., Maassab, D.S. Cho, J.J. Lai, M.H.
Kaplan, and N.W. Luckas. IL-13-induced airway hyperreactivity and mucous
production during respiratory syncitial virus (RSV) infection. J. Immunol.
166(5)3542-3548, 2001.
N.W. Lukacs, K.K. Tekkanat, A. Berlin, C.M. Hogaboam,
A. Miller, H. Evanoff, P. Lincoln, and H. Maassab. Respiratory syncitial
virus predisposes mice to augmented allergic responses via IL-13-mediated
mechanisms. J. Immunol. 167(2):2001.