Perelman School of Medicine at the University of Pennsylvania
The Beers Laboratory
Pulmonary, Allergy, and Critical Care Division of the University of Pennsylvania School of Medicine

University of Pennsylvania / School of Medicine / Beers Lab


The Beers' Laboratory for Surfactant Biology in the Pulmonary and Critical Care Division in the Department of Medicine is housed in state of the art wet bench space at the Translational Research Center of the School of Medicine at 3400 Civic Center Boulevard.  Opened in December 2011, TRC combines world class research, teaching, and animal care facilities, and is ideally positioned contiguously with the Perelman Center for Advanced Medicine at the Hospital of the University of Pennsylvania and adjacent to the Children's Hospital of Philadelphia.  This environment allows us to leverage the very best of both institutions in order to facilitate collaborative investigations in basic and translational biomedical research.

Research Portfolio of the Surfactant Biology Laboratories

The pulmonary epithelium synthesizes and secretes a surface-active film of biochemically heterogeneous lipoprotein mixture (lung surfactant) that reduces surface tension at air-liquid interfaces and allows for maintenance of alveolar stability at low lung volumes. [Figure 1] In addition two collagen-like lectin (“collectin”) protein components in surfactant are recognized for their importance in innate lung host defense and modulation of inflammation. Congenital and acquired abnormalities in surfactant component expression, in surfactant biophysics, and in the alveolar epithelial cells that produce it play an important role in the pathogenesis of adult and pediatric lung disease.

Our group is dedicated to the characterization of cellular and molecular mechanisms underlying surfactant biology and to an improved understanding of the role of the distal lung epithelium in the pathogenesis of lung disease. Current projects are focused on:

  • SP-C Mutations and Interstitial Lung Disease- We have shown that alterations in the proSP-C sequence that result in either misfolding or mistargeting of SP-C induce ER retention or formation of intracellular aggregates. Coincident with these observations, interstitial lung disease (ILD) in association with over 30 different heterozygous mutations in the SFTPC gene has been described, many of these with a structural homology with a protein associated with familial Alzheimer-like dementia (termed BRICHOS) [Figure 3].

From studies of other neurodegenerative diseases associated with mutations in proteins such as huntingin1, a-synuclein, and presenilin as well as in chronic liver disease associated with  mutant a-1 antitrypsin, the concept of ‘conformational diseases’ caused by aggregation prone mutant proteins is well-recognized.  We are currently characterizing mechanisms by which “SFTPC BRICHOS mutations” induce cell dysfunction [Figure 4] including formation of protein aggregates, generation of inflammation, and induction of apoptosis [See Movie].  Exciting new studies examining the novel role for macroautophagy in the lung for clearance of these aggregates and epithelial cytoprotection are also in progress and offer new therapeutic targets for pulmonary fibrosis. [Figure 5]






MF Beers

Michael F. Beers, M.D.
Lab Director