Professor of Medicine

Professor, Cell Biology and Anatomy, UAB

Professor, Department of Neurobiology, UAB

Professor, Department of Physiology and Biophysics, UAB

Division of Pulmonary, Allergy & Critical Care Medicine
1720 2nd Avenue So, THT-422
University of Alabama at Birmingham
Birmingham, AL 35294

Contact Information


Campus Address:


 MCLM 896

Academic Office location:


 MCLM 896

Office Phone:


 (205) 934-6439

Office Fax (Academic):


 (205) 934-1446

Email Address:



Office Assistant:   
Brynn Sharp                                
Ph: (205) 934-4304
Fax: (205) 934-1446

Brief Bio

J. Edwin Blalock, Ph.D., joined the Department of Medicine as a Professor in the Division of Pulmonary, Allergy, and Critical Care Medicine and became the Scientific Director of the Lung Health Center in 2009.  Dr. Blalock is a Distinguished Alumnus of the University of Florida where he received both a B.S. and Ph.D. degree.  He was previously a Professor in the UAB Department of Physiology and Biophysics having been recruited to UAB in 1986 from the University of Texas Medical Branch where he was a Professor of Microbiology.  Dr. Blalock is internationally recognized for his research in neuroimmunology, rational drug design, as well as the role of inflammation in chronic lung diseases.  He has published over 300 journal articles and book chapters and enjoyed uninterrupted funding for the past 32 years.  Dr. Blalock has served on two NIH study sections, as well as study sections for the American Heart Association and the National Multiple Sclerosis Society. 


Academic and Research Interest 

Unrelenting neutrophilic inflammation is a driving force in many human diseases.  Research in the Blalock laboratory has focused on understanding the cause(s) of and potential treatments for this aberrant process.  In what some consider a paradigm altering observation, the group has found that at inflammatory sites, neutrophil degradation of connective tissue proteins generates novel peptide fragments that can attract a new wave of neutrophils.  In certain individuals, it is believed that this neutrophil-mediated process becomes uncontrolled, leading to self-propagating inflammation and chronic disease.  In particular, a tripeptide (proline-glycine-proline, PGP) derived from collagen fragmentation, has been shown to attract and activate neutrophils via receptors previously thought to be only utilized by classical chemokines such as interleukin-8 (IL-8).  Moreover, chronic administration of this peptide into the airways of experimental animals causes robust neutrophil influx and a disease similar to emphysema with alveolar enlargement and right ventricular hypertrophy.  Consequently, the research has focused on airway disorders characterized by a chronic neutrophilic inflammation such as chronic obstructive pulmonary disease (COPD), cystic fibrosis (CF) and lung transplantation organ rejection.  In COPD and CF, these researchers have apparently identified a unique proteolytic pathway leading to collagen breakdown and PGP generation.  This seems to involve matrix metalloproteases (MMPs) and a novel serine protease, prolyl endopeptidase (PE); these enzymes have been found to be elevated in these disorders.  Collectively, these findings have far-reaching translational potential for human pulmonary disorders, in particular, and chronic inflammatory diseases, in general.  This is rapidly being implemented in the diagnostic arena where PGP and certain isoforms appear to be biomarkers for COPD, CF, and chronic lung transplant rejection.  Future studies will examine whether PGP and its isoforms are prognostic for disease progression and efficacy of certain therapeutic regimens.  Rational drug design has led to the development of a variety of PGP antagonists and MMP/PE inhibitors that target this novel pathway of neutrophilic inflammation and, consequently, are prototypes for drugs to treat chronic inflammatory conditions.

Key Publications

O'Reilly PJ, Jackson PL, Noerager B, Parker S, Dransfield M, Gaggar A, Blalock JE. N-alpha-PGP and PGP, potential biomarkers and therapeutic targets for COPD. Respir Res. 2009 May 18;10:38.

Hardison MT, Galin FS, Calderon CE, Djekic UV, Parker SB, Wille KM, Jackson PL, Oster RA, Young KR, Blalock JE, Gaggar A.  The presence of a matrix-derived neutrophil chemoattractant in bronchiolitis obliterans syndrome after lung transplantation. J Immunol. 2009 Apr 1;182(7):4423-31.

Gaggar A, Jackson PL, Noerager BD, O'Reilly PJ, McQuaid DB, Rowe SM, Clancy JP, Blalock JE. A novel proteolytic cascade generates an extracellular matrix-derived chemoattractant in chronic neutrophilic inflammation. J Immunol. 2008 Apr 15;180(8):5662-9.

van Houwelingen AH, Weathington NM, Verweij V, Blalock JE, Nijkamp FP, Folkerts G.  Induction of lung emphysema is prevented by L-arginine-threonine-arginine.  FASEB J. 2008; 22:3403-3408.  

Weathington NM, van Houwelingen AH, Noerager BD, Jackson PL, Kraneveld AD, Galin FS, Folkerts G, Nijkamp FP, Blalock JE.  A novel peptide CXCR ligand derived from extracellular matrix degradation during airway inflammation.  Nature Med. 2006;12:317-323.

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