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Faculty Detail Faculty Entry   
Name J EDWIN BLALOCK  
Campus Address MCLM 896 Zip 0005
Phone 205-934-6439
E-mail blalock@uab.edu" id="FacultyDetail1EmailAddress"><a href="mailto:blalock@uab.edu">blalock@uab.edu</a>
URL
 
 

Department Affiliations(s)
Appointment Type Department Division Rank
Center  Arthritis & Musculoskeletal Diseases Center  Arthritis & Musculoskeletal Diseases Center Professor
Center  Center for AIDS Research  Center for AIDS Research Professor
Center  Civitan International Research Center  Civitan International Research Center Professor
Center  Comprehensive Cancer Center  Comprehensive Cancer Center Professor
Center  General Clinical Research Center  Comprehensive Neuroscience Center Professor
Center  Cystic Fibrosis Research Center  Cystic Fibrosis Research Center Professor
Center  Medicine  Med - Cardiovascular Disease Professor
Primary  Medicine  Med - Pulmonary/Allergy/Critical Care Professor
Secondary  Cell, Developmntl, & Integrative Biology  Cell, Developmntl, & Integrative Biology Professor
Secondary  Neurobiology  Neurobiology Professor

Biographical Sketch 
J. Edwin Blalock, Professor, received his B.S. and Ph.D. degrees in 1971 and 1976, respectively,from the University of Florida. After one year postdoctoral training at the University of Texas Medical Branch, Galveston, he joined the faculty in 1977, and earned the title of Professor of Microbiology in 1984. Dr. Blalock joined the UAB faculty in 1986 as Professor of Physiology and Biophysics. Dr. Blalock joined the Department of Medicine, Division of Pulmonary, Allergy and Critical Care Medicine in 2009.

Society Memberships
Organization Name Position Held Org Link
American Association of Immunologists     
 

Research/Clinical Interest
Title
Rational Drug and Vaccine Design/Neutrophilic Inflammation
Description
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.

Postdoc Positions Available
Date Posted Position Title
No records
 

Selected Publications 
Publication PUBMEDID
Weathington, N.M., A.H. van Houwelingen, B.D. Noerager, P.L. Jackson, A.D. Kraneveld, F.S. Galin, G. Folkerts, F.P. Nijkamp, J.E. Blalock. 2006. A novel peptide CXCR ligand derived from extracellular matrix degradation during airway inflammation. Nature Med 12:317-323  16474398 
Rowe, S.M., P.L. Jackson, G. Liu, M. Hardison, A. Livraghi, G.M. Solomon, D.B. McQuaid, B.D. Noerager, A. Gaggar, J.P. Clancy, W. O'Neal, E.J. Sorscher, E. Abraham, J.E. Blalock. 2008. Potential role of high-mobility group box 1 in cystic fibrosis airway disease. Am J Respir Crit Care Med 178(8):822-831.  18658107 
Kong, M.Y., A. Gaggar, Y. Li, M. Winkler, J.E. Blalock, J.P. Clancy. 2009. Matrix metalloproteinase activity in pediatric acute lung injury. Int J Med Sci 6(1):9-17.  19159011 
Hardison, M.T., F.S. Galin, C.E. Calderon, U.V. Djekic, S.B. Parker, K.M. Wille, P.L. Jackson, R.A. Oster, K.R. Young, J.E. Blalock, A. Gaggar. 2009. The presence of a matrix-derived neutrophil chemoattractant in bronchiolitis obliterans syndrome after lung transplantation. J Immunol 182(7):4423-4431.  19299743 
O'Reilly,P., P.L. Jackson, B. Noerager, S. Parker, M. Dransfield, A. Gaggar, J.E. Blalock. 2009. N-alpha-PGP and PGP, potential biomarkers and therapeutic targets for COPD. Respir Res 10:38  19450278 
O'Reilly,P.J., M.T. Hardison, P.L. Jackson, X. Xu, R.J. Snelgrove, A. Gaggar, F.S. Galin, J.E. Blalock. 2009. Neutrophils contain prolyl endopeptidase and generate the chemotactic peptide, PGP, from collagen. J Neuroimmunol 217(1-2):51-54.  19875179 
Jackson, P.L., X. Xu, L. Wilson, N.M. Weathington, J.P. Clancy, J.E. Blalock. A. Gaggar. 2010. Human neutrophil elastase-mediated cleavage sites of MMP-9 and TIMP-1: implications to cystic fibrosis proteolytic dysfunction. Mol Med 16(5-6):159-166.  20111696 
Gaggar, A., S.M. Rowe, M. Hardison, J.E. Blalock. 2010. Proline-glycine-proline (PPG) and high mobility group box protein-1 (HMGB1): Potential mediators of cystic fibrosis airway inflammation. Open Respir Med J 4:32-38.  20448817 
Snelgrove, R.J., P.L. Jackson, M.T. Hardison, B.D. Noerager, A. Kinloch, A. Gaggar, S. Shastry, S.M. Rowe, Y.M. Shim, T. Hussell, J.E. Blalock. 2010. A critical role for LTA4H in limiting chronic pulmonary neutrophilic inflammation. Science 330(6000):90-104.  20813919 
Braber, S., P.J. Koelink, P.A. Henricks, P.L. Jackson, F.P. Nijkamp, J. Garssen, A.D. Kraneveld, J.E. Blalock. G. Folkerts. 2011. Cigarette smoke-induced emphysema in mice is associated with prolyl endopeptidase, an enzyme involved in collagen breakdown. Am J Physiol Lung Cell Mol Physiol 300(2):L255-265.  21112944 
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