Amit Gaggar, MD, MPH

Pulm_Div_Gaggar

Associate Professor of Medicine

Director, UAB Cystic Fibrosis Inflammation Group

Co-Director, Pulmonary Biospecimen Sample Repository


Division of Pulmonary, Allergy & Critical Care Medicine
1530 3rd Avenue So, THT-422
University of Alabama at Birmingham
Birmingham, AL 35294

Board Certifications
2003, American Board of Internal Medicine
2005, American Board of Internal Medicine, Pulmonary Diseases
2006, American Board of Internal Medicine, Critical Care Medicine

Medical School:  University of Michigan School of Medicine, 2000
University of Alabama - Birmingham, 2007 (PhD)

Internship:  University of Alabama - Birmingham, 2000-2001

Residency:  University of Alabama - Birmingham, 2001-2003

Fellowship:  University of Alabama - Birmingham, Pulmonary & Critical Care Medicine, 2003-2006
University of Alabama - Birmingham, Lung Transplant, 2005-2006 

Contact Information

Campus Address:

 THT 422

Academic Office location:

 MCLM 760

Office Phone:

 (205) 934-6369

Office Fax (Academic):

 (205) 934-1446

TKC Clinic Phone:

 (205) 801-7545

TKC Clinic Fax:

 (205) 802-8231

Email Address:

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Beeper #:

 8377

Office Assistant:

Amy Patillo

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Phone: (205) 975-6770 

Fax: (205) 934

Brief Bio

Dr. Gaggar obtained his medical degree from the University of Michigan in 2000 as a member of the prestigious Inteflex program.  He then moved to Birmingham, AL where he completed his internship and residency in internal medicine at the University of Alabama at Birmingham (UAB) in 2003.  Following residency training, he began fellowship training at UAB in pulmonary and critical care medicine.  During the research phase of his fellowship training, he worked in the laboratories of Dr. JP Clancy (Chief, Pediatric Pulmonology) and Dr. J. Edwin Blalock (Professor, Department of Medicine).  He completed his fellowship in 2006, with special emphasis in cystic fibrosis and lung transplantation.  The following year, Dr. Gaggar completed a PhD in Molecular and Cellular Physiology at UAB.  Dr. Gaggar was invited to joined the UAB Division of Pulmonary, Allergy & Critical Care Medicine in 2006 as instructor in medicine.  In July 2007 he was promoted to his current position as Assistant Professor of Medicine. He currently serves as a director of the Pulmonary Biospecimen Repository and the Cystic Fibrosis Inflammation Group at UAB.   He continues to see patients as both an inpatient physician and in the clinic setting.  In addition, his laboratory program continues to investigate the roles of proteases in lung disease.

Clinical Interests 

Dr. Gaggar currently sees patients after lung transplantation and individuals with cystic fibrosis at University Hospital.  He also holds a staff position at the Birmingham VA Medical Center (BVAMC) where he sees individuals with chronic obstructive lung disease (COPD).  In addition, he serves as an attending physician at both the UAB and the BVAMC intensive care units.

Academic & Research Interests

Dr. Gaggar's laboratory interests focus on the roles proteases play in modulation of lung disease.  Dr. Gaggar utilizes a combination of cell-based systems, unique murine models, and clinical specimens, leading to research which is truly "translational" in nature.  The Gaggar lab's interests focus on 3 major arenas:

(1)  Proteases and neutrophilic airway inflammation:  Recently, Dr. Gaggar's laboratory and Dr. J. Edwin Blalock's laboratory have worked together to describe the proteolytic pathways involved in the generation of a novel neutrophil chemoattractant, proline-glycine-proline (PGP).  Dr. Gaggar's group has shown that this chemoattractant is generated by the cleavage of collagen by matrix metalloprotease (MMP)-8 and MMP-9, in conjunction with a novel serine protease, prolyl endopeptidase (PE). 

Dr. Gaggar's group has also highlighted the relative contribution of PGP in development of BOS [Figure 3], demonstrating for the first time the impact this peptide might play in clinical lung disease.  Ongoing efforts are now being focused in further delineation of the biological roles PGP may induce in the airway beyond neutrophil recruitment. 

(2)  Proteases and ion transportation:  In addition to the examination of proteases in airway inflammation, Dr. Gaggar's laboratory is also examining the role of proteases in ion transport.  Recently, Dr. Gaggar's group has described a unique finding, demonstrating that specific serine proteases have the capability to reduce CFTR function [Figure 4].  These findings suggest the possibility that acquired CFTR dysfunction may be modulated via serine proteases and may play an important role
in lung diseases with a CF-like phenotype (such as chronic bronchitis).

Figure 1:  Model of PGP generation. Interaction of MMPs, PE and PGP in neutrophilic lung inflammation

Figure 2  CF sputum has capacity to generate PGP from collagen ex vivo.  CF sputum generates increased PGP from intact type I (* p<0.05) p="">

Figure 3:  PGP plays an important role in BOS.  Chemokine shift from IL-8 predominant phenotype 3 months prior to development of BOS to a PGP-predominant phenotype at time of diagnosis.  Note in both populations, PGP and IL-8 account for all chemotatic capacity of BAL fluid.

Figure 4 Human neutrophil elastase blocks CFTR dependent current in cystic fibrosis broncial epithelial monolayers (CFBE41o-)  (a). WT CFTR expressing cells were treated on their apical side with 100 ng/ml elastase for 1, 2 or 4h at 37¢ªC and Cl- secretion was assayed by the Ussing Chamber technique. The cAMP-

(3)  The Regulation of Surfactant Protein D by Airway Proteases:  D. Gaggar's group has recently characterized a mechanism by which MMP-9 can break down the collectin surfactant protein-D (SP-D), inducing changes in innate immune response.

In addition to these areas of fundamental/translational research, Dr. Gaggar continues to be involved in various phase III clinical studies in both CF and COPD patients, focusing on studies highlighting novel therapeutics targets inflammatory pathways in these conditions.  In addition, Dr. Gaggar is PI on a phase 1 study examining the role of doxycycline as a possible anti-inflammatory therapy in CF lung disease .

 

Key Publications

(1) Gaggar A, Olman, M.  Biologic markers of mortality in acute lung injury. Clin Chem Acta 372, 24-32, 2006.

(2) Gaggar A*, Li Y, Weathington N, Winkler M, Jackson PL, Blalock JE, and Clancy JP.  Matrix metalloprotease-9 dysregulation in lower airway secretions of cystic fibrosis patients.  AJP - Lung Cellular and Molecular Physiology. 293 (1): L96-L104, 2007

(3) Gaggar A*, Jackson P, Noerager B, OReilly PJ, Mcquaid DB, Rowe SM, Clancy JP, Blalock JE. A novel proteolytic cascade generates an extracellular derived neutrophil chemoattractant.  Journal of Immunology  180: 5662-5669, 2008.

(4) Hardison M, Galin FS, Calderon C, Jackson PL, Blalock JE, Gaggar A*. The presence of a matrix-derived neutrophil chemoattractant seen in bronchiolitis obliterans syndrome after lung transplantation,  Journal of Immunology 182(7), 4423-4431, 2009.

(5) O'Reilly PJ, Gaggar A*, Blalock JE.  Interfering with extracellular matrix degradation to blunt inflammation.  Current Opinion Pharmacology 8: 242-248, 2008.

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