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The Proceedings of the American Thoracic Society 5:287-289 (2008)
© 2008 The American Thoracic Society
doi: 10.1513/pats.200708-144DR
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Introduction and Perspective

David W. H. Riches, Ph.D.

Chair, 50th Annual Thomas L. Petty Aspen Lung Conference

Gregory P. Cosgrove, M.D.

Co-Chair, 50th Annual Thomas L. Petty Aspen Lung Conference

Stephen K. Frankel, M.D.

Co-Chair, 50th Annual Thomas L. Petty Aspen Lung Conference

The year 2007 saw a milestone in the history of the Thomas L. Petty Aspen Lung Conference when the 50th Annual Meeting was convened at the Given Institute, Aspen, Colorado, June 6–9. Originally conceived as the Aspen Emphysema Conference and established in 1958 by Roger Mitchell, Jack Durrance, and Giles Filey, the conference evolved in 1973 from its initial focus on obstructive lung diseases to a broader focus that included parenchymal lung disorders and specific processes and events that, when their normal homeostatic regulation goes awry, result in an impairment of lung function. Since its inception, the format of the conferences has revolved around a series of "state of the art" presentations by national and international leaders, complemented by short presentations and posters selected from the submitted abstracts. The guiding philosophy in the development of each year's program continues to be the integration of outstanding and cutting-edge clinical, translational, and basic sciences focused on a specific lung disease or process.

That being said, this year's conference on lung injury and repair represented something of a departure from the usual focus on a single lung disorder. The goal was to address the central question of why the lung repairs "normally" in some individuals after injury, yet becomes fibrotic, often progressively so, in others. By addressing this central question, we also hoped that the clinical and basic science communities would be able to embrace improved understanding of the mechanisms of lung injury and fibrosis to ultimately create better therapies. To achieve this goal, the program was focused around common aspects of both acute lung injury and idiopathic pulmonary fibrosis. Both disorders are associated with injury to the alveolar epithelium. However, whereas some individuals with acute lung injury are capable of repairing their lungs, leading to a restoration of normal structure and function, others develop an early fibrotic response that, while resulting in variable impairments of gas exchange, often lacks the relentless progression seen in patients with idiopathic pulmonary fibrosis (Figure 1). By bringing together clinical and basic scientists working on acute lung injury, idiopathic pulmonary fibrosis, and other relevant fields, we hoped to facilitate a lively dialog about the fundamental processes that are shared by these two disorders, while at the same time highlighting the differences. By discussing what is known about the underlying mechanisms of lung injury, repair, and fibrosis, our goal was to reveal more important questions about what is not known.


Figure 1
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  		Figure 1. The two central questions addressed at the Aspen Lung Conference on Lung Injury and Repair were as follows: why does acute lung injury (A; diffuse alveolar damage) result in the restoration of normal structure and function in some individuals (B; normal alveolar structure), yet leads to a severe fibroproliferative response in others (C; post–acute respiratory distress syndrome [ARDS] fibrosis); and why is the fibroproliferative response in idiopathic pulmonary fibrosis progressive (D; usual interstitial pneumonia), whereas the post-ARDS fibroproliferative response usually is not. Courtesy of Steve Groshong, M.D.

 

Figure 2
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  		Figure 2. Conference chairs and Summarizer of the 50th Meeting of the Thomas L. Petty Aspen Lung Conference. Left to right: Stephen K. Frankel, M.D. (Co-Chair), David W. H. Riches, Ph.D. (Chair), Norbert F. Voelkel, M.D. (Summarizer), and Gregory P. Cosgrove, M.D. (Co-Chair).

 

Figure 3
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  		Figure 3. The invited speakers at the 2007 Thomas L. Petty Aspen Lung Conference. Back row, left to right: Norbert Voelkel, David Schwartz, David Brenner, Skip Garcia, Bob Strieter, Barry Stripp, and David Riches. Front row, left to right: Sem Phan, Geoff Laurent, Diane Krause, Derek Radisky, Michael Matthay, Tom Martin, and Brigid Hogan.

 
The program was organized into six thematic sessions (Table 1), each of which were tethered around the processes of injury, repair, and excessive repair (fibrosis). Two of the sessions focused on the potential culprits of lung injury, including mechanical stress (Tom Martin), edema formation (Michael Matthay), and the inflammatory response (Bob Strieter). Other sessions were focused on the mechanisms of normal and abnormal repair and featured discussions of epithelial–mesenchymal transition (Derek Radisky), myofibroblast activation (Sem Phan), stem cells (Diane Krause), and the multilateral communication between epithelial, mesenchymal, and inflammatory cells and the extracellular connective tissue matrix (Geoff Laurent). Ultimately, the pursuit of scientific knowledge involves all disciplines and much can be learned from knowledge developed by parallel investigations in other organs and organisms. Several of the sessions were anchored by state-of-the-art speakers whose fields of interest extended beyond the broad areas of lung injury and repair, and their presentations served as a series of "lessons" from other systems. Normal lung injury has often been considered to be a recapitulation of lung development and Brigid Hogan and Barry Stripp discussed specific issues regarding the regulation of embryonic, neonatal, and postnatal airway epithelial development. In addition, David Brenner highlighted the intriguing similarities and differences in the mechanisms of injury and repair in the parenchyma of the liver. The final session, anchored by David Schwartz and Skip Garcia, revealed important new knowledge about the genetics of acute lung injury and pulmonary fibrosis and about the intersection between the environment and epigenetic regulation of injury and repair.


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  		TABLE 1. THEMATIC SESSIONS

 
Each Aspen Lung Conference concludes with a conference summary. This year's conference was quite unique in that, two days before the meeting, the scheduled summarizer called me to say that he was unable to travel to Aspen. After thinking this through, I called Dr. Norbert Voelkel, the chair of the 2005 Aspen Lung Conference, and asked him if he would step in at remarkably short notice to prepare and present this year's conference summary. Without hesitation, Norbert agreed and, at the conclusion of the meeting, he presented an exceptionally insightful, thoughtful, articulate, artistic, and thoroughly comprehensive summary that will be remembered for many years to come. I am deeply appreciative and indebted to Norbert for doing such a great job at very short notice.

As the Aspen Lung Conference moves into its Golden Anniversary year, it is appropriate to acknowledge that many individuals have made significant contributions to the development and success of the Aspen Emphysema Conferences and the Aspen Lung Conferences. Nobody, however, has contributed more that Dr. Tom Petty and, in 1990, the Aspen Lung Conference was renamed the Thomas L. Petty Aspen Lung Conference in recognition of Tom's enduring contributions to the continuation and success of these conferences. I have been coming to these conferences for almost 20 years, and at the beginning of most meetings Tom introduces the conference and provides a personal perspective that has ranged from the background and history of the conferences to the impact they have had on young and established investigators alike. Unfortunately, Tom was unable to make it to Aspen this year. However, the participants were surprised during the opening session with a video presentation recorded at his home a few days earlier in which Tom discussed not only the overall philosophy of the meeting but, fittingly for a conference on acute lung injury, also his personal recollections of the observations and studies that led to the original description of the adult respiratory distress syndrome in 1967 (1). These recollections are included in this issue.

The 240 participants of the 50th Thomas L. Petty Aspen Lung Conference went home invigorated by four days of convivial, lively, and stimulating discussion in the sun and snow that visited Aspen during this year's meeting. On behalf of my co-chairs, Gregory Cosgrove and Stephen Frankel, we hope that, likewise, you will enjoy, and be stimulated by, the outstanding state-of-the-art manuscripts, conference summary, and meeting abstracts that can be found in the following pages. We also hope that this will invigorate you to address new questions that will further our understanding of the mechanisms of lung injury and repair.

FOOTNOTES

Conflict of Interest Statement: D.W.H.R. received a speaking fee and travel reimbursement totaling $12,000 from Novartis for speaking at a workshop on November 29, 2005. G.P.C. does not have a financial relationship with a commercial entity that has an interest in the subject of this manuscript. S.K.F. does not have a financial relationship with a commercial entity that has an interest in the subject of this manuscript.

REFERENCES

  1. Ashbaugh DG, Bigelow DB, Petty TL, Levine BE. Acute respiratory distress in adults. Lancet 1967;2(7511):319–323.[Medline]




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