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Jerry A. Nick, M.D.

Associate Professor


 



  Jerry A. Nick, M.D.
  Associate Professor, Department of Medicine,
    National Jewish Medical and Research Center, Denver, CO
  Co-Director, Adult Cystic Fibrosis Program,
    University of Colorado Denver, Denver, CO
Associate Professor, Division of Pulmonary Science and Critical Care
  Medicine, University of Colorado Health Science Center, Denver, CO

Phone: For information and appointments to the Adult Cystic Fibrosis Clinic call Cathy Chacon, R.N. (303) 398-1178   nickj@njc.org

 

 Education & Training

Washington State University


1985 B.S., Biochemistry, Summa Cum Laude 
University of Washington School of Medicine, Seattle, WA
1989 M.D. 
1992 Internship/Residency Internal Medicine

University of Colorado School of Medicine, Denver, CO
1997 Fellowship Pulmonary/Critical Care Medicine

SOCIETIES
1997 - Present American Thoracic Society

RESEARCH INTERESTS
The primary focus of my group is the study of mechanisms that allow neutrophils (an important type of white blood cell) to respond to bacterial infections in the lung. Specifically, we have focused on a series of chemical reactions that trigger the cell's response following detection of a foreign presence in the lung or bloodstream. The inflammatory response of the neutrophils is central to both protection of the lung from diseases like bacterial pneumonia, as well as injury to the lung in diseases like cystic fibrosis. By defining the series of events that occurs prior to responses by the neutrophil, we may be able to enhance beneficial functions of the neutrophil in diseases (such as killing bacteria), and block the harmful effects of too much inflammation in diseases like septic shock, interstitial lung disease, and cystic fibrosis.

TEACHING AND PROFESSIONAL POSITIONS

Associate Director, Adult Cystic Fibrosis Program, University of Colorado Health Science Center, Denver, CO

1992 - 1993
Acting Instructor, Division of Allergy & Infectious Disease, AIDS Clinical Trial Unit, University of Washington

1997 - 2003
Assistant Professor, Department of Medicine, National Jewish Medical and Research Center, Denver, CO

1997 – 2003
Assistant Professor, Division of Pulmonary Science and Critical Care Medicine, University of Colorado Health Science Center, Denver, CO

BOARD CERTIFICATIONS
1992&2002 American Board of Internal Medicine
1996 Pulmonary
1997 Critical Care

SELECTED PUBLICATIONS

  1. Suratt, B., J. M. Petty, S. Young, K. C. Malcolm, J. Leiber, J.A. Nick, J. A. Gonzalo, P. Henson, and G. Worthen. 2004. The role of the CXCR4/SDF-1 chemokine axis in circulating neutrophil homeostasis. Blood (In Press).
  2. Nick, J. A., K. R. Poch, C. D. Coldren, M. T. Saavedra, S. Young, B. T. Suratt, P. G. Arndt, M. B. Fessler, N. J. Avdi, S. J. Gardai, K. C. Malcolm, F. J. Accurso, and M. L. Vasil. 2004. Specific Activation of Human Neutrophils by Pseudomonas aeruginosa-derived LPS: A coordinated genomics and functional analysis. Infect Immunity (Submitted).
  3. Nick, J. A., C. Coldren, M. Geraci, K. R. Poch, B. Fouty, J. O'Brien, M. Gruber, K. Kuhn, D. Richter, K. Kast, and E. Abraham. 2004. Recombinant Human Activated Protein C Reduces Human Endotoxin-induced Pulmonary Inflammation via Inhibition of Neutrophil Chemotaxis. J Clin Invest (submitted).
  4. Walker, T. S., G. S. Worthen, K. R. Poch, J. G. Lieber, M. T. Saavedra, M. L. Vasil, and J. A. Nick. 2004. Enhanced Pseudomonas aeruginosa biofilm development mediated by human neutrophils. (Submitted).
  5. Rodman, D. M., J. M. Polis, S. Heltshe, M. K. Sontag, C. Chacon, R. V. Rodman, S. Brayshaw, G. A. Huitt, Michael D. Iseman, M. T. Saavedra, L. M. Taussig, J. S. Wagener, F. J. Accurso, and J. A. Nick. 2004. Diagnosis after age thirty defines a unique population of long-term survivors of cystic fibrosis. Am J Respir Crit Care Med (Submitted).
  6. Fessler, M.B. and J.A. Nick, Cellular Signaling, in Textbook of Critical Care, M. Fink, et al., Editors. 2004 (In Press), Elsevier Science.
  7. Hanley, M.E. and J.A. Nick. 2004. Asthma and chronic obstructive pulmonary disease. In: Primary Care Secrets, 3rd Ed. Mladenovic, J. (Ed.), Hanley & Belfus, Inc., Philadelphia.440-7.
  8. Hanley, M.E. and J.A. Nick, 2004. Hypoxemia and oxygen therapy. In: Primary Care Secrets, 3rd Ed. Mladenovic, J. (Ed.), Hanley & Belfus, Inc., Philadelphia. 451-6.
  9. Saavedra, M., J.A. Nick. 2003 Chronic Bronchiectasis and Cystic Fibrosis. In Current Diagnosis and Treatment in Pulmonary Disease, Eds M. Hanley and C. Welch. McGraw-Hill. 92-104.
  10. Nick, J.A. 2003 Atypical Mycobacteria. In “Cystic Fibrosis and Bronchiectasis” Seminars in Respiratory and Critical Care Medicine, Ed. Bruce K. Rubin, Editor-in-Chief Joseph Lynch. 24(6); 693-702.
  11. Taube, C., J.A. Nick, B. Siegmund, C. Duez, K. Takeda, Y.H. Rha, J.W. Park, A. Joetham, K. Poch, A. Dakhama, C.A. Dinarello, E.W. Gelfand. Inhibition of early airway neutrophilia does not affect development of airway hyperresponsiveness. Am J Respir Cell Mol Biol, 2004 (In Press).
  12. Gardai, S.J., Y.Q. Xiao, M. Dickinson, J.A. Nick, D.R. Voelker, K.E. Greene, P.M. Henson. By binding SIRPalpha or calrecticulin/CD91, lung collectins act as duel function surveillance molecules to suppress or enhance inflammation. Cell, 2003. 115(1): p. 13-23.
  13. Taube, C., A. Dakhama, Y. H. Rha, K. Takeda, A. Joetham, J.W. Park, A. Balhorn, T. Takai, K.R. Poch, J. A. Nick, and E. Gelfand. 2003. Transient Neutrophil Inflammation After Allergen Challenge is Dependent on Specific Antibodies and Fcg Receptors. J Immunol, 170(8) 4301-9.
  14. Nick, J. A., S. K. Young, P. G. Arndt, J. G. Lieber, B. T. Suratt, K. R. Benchich, N. J. Avdi, K. C. Malcolm, C. Taube, P. M. Henson, and G. S. Worthen. 2002. Selective Suppression of Neutrophil Accumulation in Ongoing Pulmonary Inflammation by Systemic Inhibition of p38 MAP Kinase. J Immunol, 169(9) 5260-69.
  15. Avdi, N. J., K. C. Malcolm, Nick, J. A., and G. S. Worthen. 2002. A role for PP2A in p38 Mitogen-activated Protein Kinase-mediated Regulation of the c-Jun NH2-terminal Kinase Pathway in Human Neutrophils. J Biol Chem, 277(43),40687-96..
  16. Suratt, B., S.K. Young, J. Lieber, J. A. Nick, P.M. Henson, G. S. Worthen. 2001. Neutrophil maturation and activation determine anatomic site of clearance from circulation. Am J Physiol Lung Cell Mol Physiol, 281(4):L913-21.
  17. Avdi, N.J., J. A Nick, B. B. Whitlock, M. A. Billstrom, P. M. Henson, G. L. Johnson, G. S. Worthen. 2001. TNFa activation of the c-Jun NH2-terminal Kinase (JNK) pathway in human neutrophils: Integrin involvement in a pathway leading from cytoplasmic tyrosine kinase to apoptosis. J Biol Chem, 276(3),2189-99.
  18. Nick, J. A., S. K. Young, K. K. Brown, N. J. Avdi, P. G. Arndt, B. T. Suratt, M. Janes, P. M. Henson and G. S. Worthen. 2000. Role of p38 MAP Kinase in a Murine Model of Pulmonary Inflammation. Journal of Immunology : 164:2151-2159.
  19. Nick, J. A., N. J. Avdi, S. K. Young, L. A. Lehman, P. P. McDonald, S. C. Frasch, M. A. Billstrom, P. M. Henson, G. L. Johnson and G. S. Worthen. 1999. Selective activation and functional significance of p38a mitogen-activated protein kinase in lipopolysaccharide-stimulated neutrophils. Journal of Clinical Investigation. 103:851-858.
  20. Nick, J. A., D. A. Lynch, M. I. Schwarz and M. E. Hanley. 1999. A Thoracic Complication of Hereditary Multiple Exostoses. Respiratory Medicine. 93:217-219.
  21. Frasch, S. C., J. A. Nick, F. V. A, D. L. Bratton, G. S. Worthen and P. M. Henson. 1998. p38 Mitogen-activated Protein Kinase-dependent and -independent Intracellular Signal Transduction Pathways Leading to Apoptosis in Human Neutrophils. Journal Biological Chemistry. 273:8389-8397.
  22. Nick, J. A., N. J. Avdi, S. K. Young, C. Knall, G. L. Johnson and G. S. Worthen. 1997. Common and distinct intracellular signaling pathways in human neutrophil utilized by platelet activating factor and FMLP. Journal of Clinical Investigation. 99:975-986.
  23. Nick, J. A., N. J. Avdi, P. Gerwins, G. L. Johnson and G. S. Worthen. 1996. Activation of a p38 mitogen-activated protein kinase in human neutrophils by lipopolysaccharide. Journal of Immunology. 156:4867-4875.
  24. Knall, C., S. Young, J. A. Nick, A. M. Buhl, G. S. Worthen and G. L. Johnson. 1996. Interleukin-8 regulation of the ras/raf/mitogen-activated protein kinase pathway in human neutrophils. Journal Biological Chemistry. 271:2832-2838.
  25. Nick, J. A., R. Tuder, R. May and J. Fisher. 1996. Polyarteritis Nodosa with Pulmonary Vasculitis. American Journal of Respiratory and Critical Care Medicine. 153:450-453.
  26. Schwarz, M. I., J. M. Sutarik, J. A. Nick, J. A. Leff, J. W. Emlen and R. M. Tuder. 1995. Pulmonary Capillaritis and Diffuse Alveolar Hemorrhage, A Primary Manifestation of Polymyositis. American Journal of Respiratory and Critical Care Medicine. 151:2037-204

BOOK CHAPTERS AND REVIEWS

  1. Vourlekis, J. S., J. A. Nick and T. L. Petty. 1999. Pleuropulmonary Disease, Hepatosplenomegaly, and Severe Anemia in A 23-Year-Old Peace Corps Worker. Cortlandt Forum . Dec:231-236
  2. Nick, J. A., N. J. Avdi, S. K. Young, P. P. McDonald, M. A. Billstrom, P. M. Henson, G. L. Johnson and G. S. Worthen. 1999. An Intracellular Signaling Pathway Linking LPS Stimulation To Cellular Responses of the Human Neutrophil: The p38 MAP Kinase Cascade and Its Functional Significance. Chest. 116:54-55S.
  3. Hanley, M. E. and J. A. Nick. 1998. Asthma and Chronic Obstructive Pulmonary Disease. In Primary Care Secrets. Eds J. Mladenovic. Hanley & Belfus. Philadelphia. 384-391
  4. Hanley, M. E. and J. A. Nick. 1998. Hypoxemia and Oxygen Therapy. In Primary Care Secrets. Eds J. Mladenovic. Hanley & Belfus. Philadelphia. 395-399
  5. Worthen, G. S. and J. A. Nick. 1998. Leukocyte Accumulation in the Lung. In Pulmonary Diseases and Disorders. Eds A. P. Fishman. McGraw-Hill. New York. 325-336

MANUSCRIPTS SUBMITTED OR IN PREPARATION

  1. Nick, J. A., S. K. Young, P. G. Arndt, J. G. Lieber, B. T. Suratt, K. R. Benchich, N. J. Avdi, K. C. Malcolm, C. Taube, P. M. Henson, and G. S. Worthen. 2002. Selective Suppression of Neutrophil Accumulation in Ongoing Pulmonary Inflammation by Systemic Inhibition of p38 MAP Kinase. J Immunol (submitted).

RESEARCH
Pro-Inflammatory Stimulation and Intracellular Signaling Pathways in the Human Neutrophil

Research Assistants:
Katie Poch
Travis Walker
Fellow:
Chris Gregory, M.D.

Many pulmonary diseases are characterized by a massive accumulation of neutrophils in the airspaces. The recruitment of neutrophils to the lung is a central part of the innate host defense against infection. However, in certain conditions, such as the Acute Respiratory Distress Syndrome (ARDS) and Cystic Fibrosis, it appears that the actions of the neutrophils are injurious to the airways. Other infections, such as those caused by mycobacteria, appear to evoke very little neutrophil response. Over the past decade, intensive efforts have been focused at inhibiting neutrophil responses that appear to be "overexuberant" in diseases that feature intense inflammation.

External stimulation and subsequent functional responses of eukaryote cells are linked through a series of intracellular phosphorylation events that form signal transduction pathways. In the neutrophil, pro-inflammatory stimuli selectively evoke a range of common and unique functional responses. We have studied in depth the p38 mitogen-activated protein kinase (MAPK) pathway that is utilized by human neutrophils in response to a wide range of clinically important pro-inflammatory stimuli. We have found that a broad spectrum of neturophil responses are mediated by p38 MAPK, and that this signaling mechanism can serve both as a regulator of cell response and a marker of cellular activation. With newly available inhibitors, which selectively block the activation of p38 MAPK, this molecule represents a potential target for development of anti-inflammatory agents.

A second focus of our group is to study the coordination of neutrophil responses. From the first seconds of stimulation to the ultimate death of the cell, the neutrophil undergoes a series of responses that can either be “pre-programmed” or “selective”. Responses include neutrophil adhesion, chemotaxis, release of oxygen radicals, release of preformed granule proteins, transcription of RNA, de novo synthesis of proteins, phagocytosis, and ultimately necrosis or apoptosis of the cells. Although much is known about each of these responses, very little is known of how these responses are coordinated. Through a combined functional, signaling, and genomic analysis, we are examining the coordinated response of the neutrophil to LPS in the setting of acute lung injury, and the response of the neutrophil to Pseudomonas aeruginosa in the setting of Cystic Fibrosis lung disease. In addition, we are examining the response of the Pseudomonas to the neutrophil, in the context of bacterial survival and biofilm development. Through these analyses, we can now identify features of the neutrophil response characteristic of these diseases, and test the relative effect of various promising anti-inflammatory agents.





Signal Transduction Figure: Example of how stimulation of the neutrophils by clinically important pro-inflammatory stimuli such as LPS and TNF-a induce a sequence of intracellular signaling events leading to activation of p38 MAPk, which in turn results in a broad range of functional responses.