Grunig Lab

Gabriele Grunig, DVM, Ph.D.

Professor, Department of Environmental Medicine
and Medicine (Pulmonary Medicine)

Contact Info:

Address: 57 Old Forge Road, Tuxedo, NY 10987
PHL building, 8th floor, 455 First Ave, New York, NY 10016
Phone: 845-731-3669; 917-826-3618
Email: Gabriele.Grunig@nyumc.org

 

Key Interests

Lung diseases associated with environmental pollutants: asthma, pulmonary hypertension, chronic inflammation, airway and arterial remodeling; Interactions between the immune system and environmental pollutants; Soluble mediators (cytokines such as IL-13, IL-10 family cytokines)

Biographic Details:

Graduate Education:
1982-1984 — Veterinary Med Univ of Zurich
1990-1994 — Cornell U

Postdoctoral Training:
1994-1998 DNAX Research Institute, Palo Alto, CA
1998-1999 University of California, San Francisco, CA

Academic Appointments:

2000-2006: Assistant Professor of Pathology, Columbia University / St. Luke's Roosevelt Hospital, New York, NY
2006-2008: Assistant Professor of Microbiology, Columbia University, New York, NY
2008-2010: Assistant Professor of Environmental Medicine, NYU Medical Center, New York, NY
Since 2010: Associate Professor of Environmental Medicine and Medicine, NYU Medical Center, New York, NY

Major Responsibilities:
2002-2005 Director of the mouse asthma model lung physiology Core for the Columbia University Asthma P01 grant

Research Interests:

The work in the Grunig Lab is focused on chronic lung diseases (asthma, pulmonary hypertension) that are exacerbated by air pollution.  We have currently major funding by the NIH, and private foundations to study the mechanisms that cause pulmonary hypertension (the increase in the pressure of the blood that is pumped through the lungs), and the remodeling of the blood vessels of the lungs.  In our laboratory, we work with mouse models of the disease and human blood samples.  We use physiology (e.g. right heart catheterization); immunology (e.g. blocking antibodies, flow cytometry); and molecular biology tools (e.g. qPCR, microRNA antagomirs, array technology).  

Exposure to airborne pollutants and cigarette smoke are major causes of chronic inflammation in the lungs. The lungs also become more susceptible to infection with viruses or bacteria. The result is the dysfunction of the bronchi that transport air to and from the alveoli, and to the blood vessels that circulate the blood through the lungs. The major focus point of research in the laboratory is to define the role of secreted proteins by which immune cells communicate with the cells that make up the structure of the lungs. This research has identified one of these mediators, called Interleukin-13 (IL-13), to directly initiate the processes that induce the cardinal signs of asthma: bronchial constriction, inflammation and increased mucus production.  Currently, we are collaborating with faculty members at the NYU Medical Center to determine identify additional mechanisms that cause the asthma phenotype. 
We have most recently begun to investigate the blood vessels in the lungs. We have shown for the first time experimentally that the immune response can induce severe wall-thickening of arteries (structure stained in brown by labeling with a smooth muscle specific antibody) in the lungs. In addition, the studies showed that Interleukin-13 (IL-13) is a critical, indirect communicator in the process that leads to the severe thickening of the pulmonary arterial walls. This thickening of the pulmonary arterial walls has been described in patients who have pulmonary hypertension, a debilitating disease that frequently accompanies chronic lung disease caused by smoking.  Our studies have found that particulate matter from air pollution collected in New York City exacerbates the response to antigen exposure and induces the pulmonary hypertension phenotype with significantly increased pressures in the right ventricle, and increased pulmonary arterial remodeling.  We are now identifying the immune mechanism and the changes in micro-RNA expression that cause the pulmonary hypertension phenotype.

This research might aid in developing new methods to follow disease progression and tailor treatment strategies in patients with chronic lung disease such as asthma and pulmonary hypertension.

Selected Publications:

Pulmonary Arterial Remodeling Induced by a Th2 Immune Response. Daley, E; Emson, C; Guignabert, C; de Waal Malefyt, R; Louten, J; Kurup, VP; Hogaboam, C; Taraseviciene-Stewart, L; Voelkel, NF; Rabinovitch, M; Grunig, E; Grunig, G. J Exp Med 2008; 205: 361-372.

Prenatal allergen and diesel exhaust exposure and their effects on allergy in adult offspring mice. Lin, L; Zhu, H; Quan, C; Grunig, G; Ballaney, M; Jin, X; Perera, FP; Factor, PH; Chen, LC; Miller, RL. Allergy Asthma Clin. Immunol. 2010, 6:7.

Exposure to Inhaled Nickel Nanoparticles Causes a Reduction in Number and Function of Bone Marrow Endothelial Progenitor Cells. Liberda, EN; Cuevas, AK; Gillespie, P; Grunig, G; Qu, Q; Chen, LC. Inhal Toxicol. 2010, 22 Suppl 2:95-9. ISI Cited 1

Interleukin-19: a constituent of the regulome that controls antigen presenting cells in the lungs and airway responses to microbial products. Hoffman, C; Park, SH; Daley, E; Emson, C; Louten, J; Sisco, M; de Waal Malefyt, R; Grunig, G. PLoS One. 2011;6: e27629. Faculty of 1000 ranking: FFa 8, novel drug target, new finding.

Prenatal exposure to allergen and DNA methylation, allergy in grandoffspring mice. Niedzwiecki, M; Zhu, H; Corson, L; Grunig, G; Factor, PH; Chu, S; Jiang, H; Miller, R.L. Allergy 2012, 67: 904-910.

Interleukin 13 and the evolution of asthma therapy. Grunig, G; Corry, DB; Reibman, J; Wills-Karp, M Am J Clin Exp Immunol 2012; 1(1):20-27.

Right ventricular systolic pressure measurements in combination with harvest of lung and immune tissue samples in mice. Chen, W.C.*, Park, S.H.*, Hoffman, C., Philip, C., Robinson, L., West, J., Grunig, G. Right J Vis Exp. 2013 Jan 16;(71). *both authors contributed equally.

Modification of hemodynamic and immune responses to exposure with a weak antigen by the expression of a hypomorphic BMPR2 gene. Park, S.H., Chen, W.C., Hoffman, C., Marsh, L.M., West, J., Grunig, G. PLoS One. 2013;8(1):e55180. Epub 2013 Jan 29.

MicroRNA-375 Regulation of Thymic Stromal Lymphopoietin by Diesel Exhaust Particles and Ambient Particulate Matter in Human Bronchial Epithelial Cells.  Bleck, B., Grunig, G., Chiu, A., Liu, M., Gordon, T., Kazeros, A., Reibman, J.  J Immunol. 2013 Mar 1. [Epub ahead of print]

IL-13 and IL-17A/F induce the pulmonary hypertension phenotype caused by exposure to antigen and urban particulate air pollution.  Park, SH; Chen, WC; Hoffman, C; Gordon, T; Grunig, G. In preparation.

Selected Abstracts:

Adaptive immune response in pulmonary hypertension. 
Grunig, Gabriele; Chen, Wen-Chi; Hoffman, Carol; Gordon, Terry; Park, Sung-Hyun. 2012 MAY 1;188:-, Journal of immunology.— id: 169547, year: 2012, vol: 188, page: , stat: Journal Article,

Prenatal exposure to allergen, DNA methylation, and allergy in grandoffspring mice. Niedzwiecki, M; Zhu, H; Corson, L; Grunig, G; Factor, P H; Chu, S; Jiang, H; Miller, R L. 2012 Jul;67(7):904-910, Allergy.— id: 169708, year: 2012, vol: 67, page: 904, stat: Journal Article,

L-33 upregulate myeloid DC maturation induced by diesel-exhaust particle treated human bronchial epithelial cells. Bleck, B; Ahsan, M R; Tse, D B; Grunig, G; Reibman, J. 2011 01 May 2011;183(1):-, American journal of respiratory & critical care medicine.— id: 177200, year: 2011, vol: 183, page: , stat: Journal Article,

The role of relma (Resistin like molecule a) in the responses of the lung's vasculature to antigen and urban particulate matter. Grunig, G; Hoffman, C; Sisco, M; Bleck, B; Gordon, T; Reibman, J. 2011 01 May 2011;183(1):-, American journal of respiratory & critical care medicine.— id: 177190, year: 2011, vol: 183, page: , stat: Journal Article,

See All Publications

Lab Members:

Wen-Chi Chen, MS  (laboratory manager)
Sung-Hyun Park, PhD (postdoctoral fellow)
Nafiseh Esmaeil (visiting PhD student from Isfahan, Iran)
Katelin Jackson (summer student)