Nicholas Lukacs, Ph.D.
Nicholas W. Lukacs is the Godfrey D. Stobbe Professor of Pathology at the University of Michigan Medical School in Ann Arbor, Michigan. He received his Ph.D. from Wayne State University in 1992 and was first appointed as a faculty member at the University of Michigan in 1994. He also serves as an Assistant Dean for Faculty Affairs at the University of Michigan Medical School. Most recently, Dr. Lukacs has taken the role as Scientific Director of the Mary H Weiser Food Allergy Center. Presently, his research funding includes National Institute of Health grants, as well as pharmaceutical research contracts. He has served on editorial boards of numerous journals and as a reviewer for NIH and Foundation grant study sections. Dr. Lukacs has co-authored over 280 peer-reviewed publications and greater than 40 invited book chapters and reviews. The Lukacs Lab research is presently focused on the innate and acquired immune responses in allergen- and respiratory virus-induced acute and chronic diseases, as well as the role that the gut microbiome has on development of allergic diseases. Studies in the laboratory have been focused on the function and activation of DC and T cells during infections and the differential epigenetic modulation of the immune and pathologic responses that lead to exacerbated disease progression. Translational collaborations include studies examining severe respiratory syncytial virus (RSV)-induced disease with infants in the Pediatric ICU and development of food and airborne allergen responses in inner city birth cohorts with collaborators from Henry Ford Medical Center and UCSF. More recently collaborative studies have been initiated in children with Eosinophilic Esophagitis (EoE) with U of Michigan cohorts conducted by Dr. Vera Dematos from Pediatric Gastroenterology. In the laboratory, a new model of EoE has been established in collaboration with Dr. Catherine Ptaschinski, Ph.D. to correlate clinical findings with specific mechanisms of action.
Over the past several years our laboratory research has focused on the interrelationship of cytokines, chemokines, and leukocyte activation during asthmatic-type airway and Th1/Th2 type immune responses. The development of a clinically relevant mouse cockroach allergen-induced airway model that demonstrates a number of in vivo correlates to human asthma has been successfully utilized to further elucidate novel mechanisms of pulmonary inflammation. The areas that have been successfully investigated using the allergic airway models include mast cell biology, eosinophilic inflammation, and T lymphocyte activation. In addition, we also examine the role of pulmonary viral infections (Respiratory Syncytial Virus; RSV) on exacerbation and increased development of allergic asthmatic responses. Using these models, we have specifically identified particular leukocyte populations that have an effect during different stages of asthmatic-like responses within the lung. Our most recent research has centered upon the role of important innate immune molecules that direct the direction of the immune response using defined mechanisms of activation. In particular, the toll-like receptor (TLR) system and a novel Notch ligand mediated activation of T lymphocytes has led to a number of important mechanistic studies.
Mukherjee, S., DM Lindell, AA Berlin, SB Morris, TP Shanley, MB Hershenson, and NW Lukacs. IL-17-induced pulmonary pathogenesis during respiratory viral infection and exacerbation of allergic disease. Amer. J. Pathol. 2011. 179(1):248-58.
Morris, S., MS Swanson, A Lieberman, M. Reed, Z. Yue, DM Lindell, and NW Lukacs. Autophagy-mediated DC activation is essential for innate cytokine production and APC function with Respiratory Syncytial Virus responses. J. Immunol. 187(8):3953-61 2011.
Petersen BC, Budelsky AL, Baptist AP, Schaller MA, Lukacs NW. IL-25 induces type 2 cytokine production in a novel, steroid resistant IL-17RB+ myeloid population that exacerbates asthmatic pathology. Nature Medicine. 2012 Apr 29. 18(5):751-8
Demoor T, Petersen BC, Morris S, Mukherjee S, Ptaschinski C, De Almeida Nagata DE, Kawai T, Ito T, Akira S, Kunkel SL, Schaller MA, Lukacs NW. IPS-1 signaling has a nonredundant role in mediating antiviral responses and the clearance of respiratory syncytial virus. J. Immunol. 2012, 189:5942-53.
Reed M, Morris SH, Jang S, Mukherjee S, Yue Z, and Lukacs NW. Autophagy-inducing protein Beclin-1 dendritic cells regulate CD4 T cell responses and disease severity during Respiratory Syncytial Virus Infection. 2013. J. Immunol. 191:2526-37.
Fujimura KE, Demoor T, Rauch M, Faruqi AA, Jang S, C Johnson C, Boushey HA, Zoratti E, Ownby D, Lukacs NW*, Lynch SV: House dust exposure mediates gut microbiome Lactobacillus enrichment and airway immune defense against allergens and virus infection. Proceedings of the National Academy of Sciences of the United States of America: 111(2):805-10. 2014. (*co-corresponding author)
de Almeida Nagata DE, Demoor T, Ptaschinski C, Ting HA, Jang S, Reed M, Mukherjee S, Lukacs NW: IL-27R-Mediated Regulation of IL-17 Controls the Development of Respiratory Syncytial Virus Associated Pathogenesis. The American journal of pathology: 184(6):1807-18. 2014.