New Ways to Tackle COPD and Other Chronic Pulmonary Diseases


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WEDNESDAY, NOVEMBER 3

12:20 - 1:30 pm Conference Registration

 

New Pathways And Molecular Targets For Treating COPD

1:30 Chairperson’s Remarks

 

1:40 KEYNOTE PRESENTATION: Overcoming Steroid Insensitivity in COPD 

Ian AdcockIan Adcock, Ph.D., Professor, Respiratory Cell & Molecular Biology, Airways Disease Section, National Heart and Lung Institute and Faculty of Medicine, Imperial College, London 

COPD is characterized by an enhanced and uncontrolled inflammatory response. Crucially, COPD is poorly controlled by current anti-inflammatory therapies including glucocorticoids. Elevated lung oxidant burden and activation of key pathways that impinge upon GR function such as p38 MAPK, NF-κB and IL-17 may drive this insensitivity. In addition, the expression and activity of the GR co-repressor protein histone deacetylase 2 (HDAC2) is reduced in COPD in response to oxidative stress possibly due to elevation of the phosphoinositol 3-kinase (PI3K)δ signaling pathway. Importantly, blockade of PI3Kδ or p38 MAPK in primary cells from disease or in disease models restores glucocorticoid function. Selective inhibition of these pathways may provide a therapeutic strategy in COPD both as a novel anti-inflammatory and as a combinatorial therapy with glucocorticoids.

2:40 Autophagy in COPD 

Augustine Choi, M.D., Department of Medicine, Harvard Medical School and Chief, Pulmonary and Critical Care Medicine, Brigham And Women’s Hospital

Chronic obstructive pulmonary disease (COPD) is a debilitating disease caused by chronic exposure to cigarette smoke (CS), which involves airways obstruction and alveolar loss (emphysema). Our previous studies demonstrated elevated autophagy in human COPD lung, and as a cellular and tissue response to CS exposure in experimental model of emphysema in vivo. We identified the autophagic protein microtubule associated protein-1 light chain-3B (LC3B) as a positive regulator of CS-induced lung epithelial cell death. We now extend these initial observations to explore the mechanism by which LC3B mediates CSinduced apoptosis and emphysema development in vivo. Here, we observed that LC3B-/- mice demonstrated significantly decreased levels of apoptosis in the lungs after CS exposure, and displayed resistance to CS-induced airspace enlargement, relative to wild-type littermate mice. We found that LC3B associated with the extrinsic apoptotic factor Fas in lipid rafts in an interaction mediated by caveolin-1 (Cav-1). The siRNA-dependent knockdown of Cav-1 sensitized epithelial cells to CS-induced apoptosis, as evidenced by enhanced DISC formation and caspase activation. In conclusion, we demonstrate a pivotal role for the autophagic protein LC3B in CS-induced apoptosis and emphysema, suggestive of novel therapeutic targets for COPD treatment.    

3:10 Networking Refreshment Break in the Exhibit Hall
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3:45 Talk Title to be Announced

J. David Farrar, Ph.D., Associate Professor, Department of Immunology, University of Texas Southwestern Medical Center

4:15 Sponsored Presentation (Opportunity Available)

4:45 A Decoy CXCL8 Shows Potent Anti-Inflammatory Activity in Murine Lung Inflammation Models of COPD

Andreas J. Kungl, Ph.D., CSO, ProtAffin Biotechnologie AG

Neutrophils play a fundamental role in several chronic lung diseases including COPD and cystic fibrosis. Among the mediators of neutrophil recruitment into the lung, the chemokine CXCL8 is considered to be the major player. CXCL8 exerts its chemotactic activity by binding to its GPCR receptors located on the neutrophils, as well as through interactions with co-receptors located on the inflamed endothelium, the socalled glycosaminoglycans (GAGs). We have engineered higher affinity for GAG binding into human CXCL8 thereby obtaining a protein-based inhibitor for the CXCL8/GAG interaction. By additionally knocking-out the GPCR domain of the chemokine, we obtained a decoy protein (termed PA401) with potent anti-inflammatory characteristics. PA401 has been tested in murine models of lung inflammation induced by lipopolysaccharide and tobacco smoke in which the compound showed strong dose-dependent reduction of BAL neutrophils after intravenous and subcutaneous administration at doses of 40 and 400μg/kg. PA401 is therefore considered a new promising biologic therapeutic with a novel mechanism of action for interfering with lung inflammation.    

5:15 PANEL DISCUSSION: What Are the Biggest Challenges in COPD Over the Next Decade?

Moderator: Augustine Choi, M.D., Department of Medicine, Harvard Medical School and Chief, Pulmonary and Critical Care Medicine, Brigham and Women’s Hospital

5:45 End of Day


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SPONSORSHIPS & EXHIBITS 

The exhibit hall was sold out in 2013, so please contact us early to reserve your place. To customize your sponsorship or exhibit package for 2014, contact:

Jon Stroup
Business Development Manager
781-972-5483
jstroup@healthtech.com