Pulmonary and Critical Care Medicine

Physician Photo

Barry S. Shea, MD

  • Phone: 617-726-1721
Pulmonary and Critical Care Medicine
Department of Medicine


  • Critical Care Center
  • Medical Intensive Care Unit
  • Cardiac Intensive Care Unit
Clinical Interests
Pulmonary Fibrosis
Lung injury
Critical care
Interstitial lung disease
Boston: Massachusetts General Hospital
Medical Education
MD, Tufts University School of Medicine
Residency, Cornell University Medical Center
Fellowship, Cornell University Medical Center
Fellowship, Massachusetts General Hospital
Board Certifications
Pulmonary Disease, American Board of Internal Medicine
Critical Care Medicine, American Board of Anesthesiology
Patient Age Group
Accepting New Patients


Dr. Shea's primary research objective is to achieve better understanding of the biological mechanisms underlying the development of pulmonary fibrosis, with the hope that such knowledge will lead to new therapies for fibrotic lung diseases.  Idiopathic pulmonary fibrosis (IPF), the quintessential fibrotic lung disease, is in dire need of scientific breakthroughs.  IPF is a disease of unknown etiology characterized by progressive scar formation in the lungs, leading to impaired lung function, difficulty breathing, and in many cases death.  The therapeutic options for patients with IPF and other forms of pulmonary fibrosis are limited.  Dr. Shea's basic science research is currently focused on two lysophospholipid mediators, lysophosphatidic acid (LPA) and sphingosine 1-phosphate (S1P), which appear to be critical regulators of the development of lung fibrosis.  Dr. Shea has also established a translational research program in interstitial lung diseases (ILDs) at MGH, the primary goals of which are to 1) identify potential biomarkers which may predict disease progression in IPF and other ILDs and 2) discover novel pathways involved in the pathogenesis of lung fibrosis.


Tager AM, LaCamera P*, Shea BS*, Campanella GK, Selman M, Zhao Z, Polosukhin V, Wain J, Karimi-Shah BA, Kim ND, Hart WK, Pardo A, Blackwell TS, Xu Y, Chun J, Luster AD. The lysophosphatidic acid receptor LPA1 links pulmonary fibrosis to lung injury by mediating fibroblast recruitment and vascular leak. Nat Med 2008;14(1):45-54.

Shea BS, Brooks SF, Fontaine BA, Chun J, Luster AD, Tager AM. Prolonged exposure to sphingosine 1-phosphate receptor-1 agonists exacerbates vascular leak, fibrosis, and mortality after lung injury. Am J Resp Cell Mol Biol 2010;43(6):662-73.

Liu F, Mih JD, Shea BS, Kho AT, Sharif AS, Tager AM, Tschumperlin DJ. Feedback amplification of fibrosis through matrix stiffening and COX-2 suppression. J Cell Biol 2010;190(4):663-706.

Hariri LP, Mino-Kenudson M, Shea B, Digumarthy S, Onozato M, Yagi Y, Fraire AE, Matsubara O, Mark EJ. Distinct histopathology of acute onset or abrupt exacerbation of hypersensitivity pneumonitis. Hum Path 2012;43(5):660-8.

Shea BS and Tager AM. Role of the lysophospholipid mediators lysophosphatidic acid and sphingosine 1-phosphate in lung fibrosis. Proc Am Thorac Soc 2012;9(3):102-110.

Shea BS and Tager AM. Sphingolipid regulation of tissue fibrosis. Open Rheum 2012;6:123-9.

Pulmonary and Critical Care
55 Fruit Street
Boston, MA 02114-2696

Phone: 617-726-1721
Fax: 617-726-6878