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Introduction

University of Nebraska Medical Center Omaha, Nebraska

Tim Higenbottam

AstraZeneca R&D Charnwood, Loughborough, United Kingdom

Not so long ago, emphysema was regarded as irreversible. The demonstration that this is not the case, and that the adult mammalian lung can form new alveolar wall after the development of emphysema (1), has opened entirely new avenues to approach the therapy of chronic obstructive pulmonary disease (COPD). Although simple administration of all trans-retinoic acid reversed emphysema in the young adult rat, limited trials have suggested that it will be more complicated in the human disease (2). Understanding the key issues involved in lung repair will likely require integration of areas of study that have been previously disparate.

The Lund COPD Symposia are annual meetings sponsored by AstraZeneca. While the company maintains a major commitment to the development of products for the treatment of COPD, the symposia are not directly related to any specific corporate agenda. Rather, the symposia have focused on the scientific areas where research in COPD is advancing and where a symposium will help facilitate the exchange and maturation of key new concepts. It was in this context that the topic for the Sixth Annual Symposium, "Tissue Remodeling and Repair Mechanisms in COPD," was conceived.

Whether tissue remodeling and repair recapitulates development is an area of active research interest, and the Sixth Symposium began with a keynote presentation on lung development, an area that has seen rapid growth in the understanding of the molecular events involved. The symposium continued with sessions dedicated to remodeling of the pulmonary vasculature, of the airways, and of the alveolar wall. Finally, the symposium included a second keynote presentation addressing the role of programmed cell death in tissue maintenance, repair, remodeling, and in inflammatory diseases such as COPD.

The actual symposium included lively discussions, and the current set of reviews includes a summary, prepared by Prof. Alan Leff, that attempts to capture some of the content and enthusiasm present during the meeting in Lund. What is clear is that COPD can no longer be regarded as an "irreversible" condition. The cellular and biochemical processes that lead to tissue alteration in COPD are all potentially reversible. Developing therapies to reverse COPD may be a long-term project. However, understanding the pathways involved and how to exploit the therapeutic opportunities offered promises to be an active area of research in the coming years. Both the advancing biology and the great potential to address the problems faced by patients with COPD should make the reviews that follow, which were derived from the presentations made in Lund, of interest to both the researcher and the clinician.

FOOTNOTES

Conflict of Interest Statement: S.I.R. has participated as a speaker in scientific meetings and courses under the sponsorship of AstraZeneca and GlaxoSmithKline. He serves on Advisory Boards for Altana, AstraZeneca, Dey, GlaxoSmithKline, and Inspire. He has conducted clinical trials for AstraZeneca, Centocor, GlaxoSmithKline, Pfizer, Roche, and Sanofi. He has served as a consultant for AstraZeneca, GlaxoSmithKline, Novartis, Pfizer, and Roche. A patent is pending on the use of PDE4 inhibitors in repair; he is a co-inventor of the patent owned by the University of Nebraska Medical Center. T.H. is employed by AstraZeneca in R&D Charnwood and Lund (UK & Sweden).

REFERENCES

1. Massaro G, Massaro D. Retinoic acid treatment abrogates elastase-induced pulmonary emphysema in rats. Nat Med 1997;3:675–677.[CrossRef][Medline]
2. Mao JT, Goldin JG, Dermand J, Ibrahim G, Brown MS, Emerick A, McNitt-Gray MF, Gjertson DW, Estrada F, Tashkin DP, et al. A pilot study of all-trans-retinoic acid for the treatment of human emphysema. Am J Respir Crit Care Med 2002;165:718–723.[Abstract/Free Full Text]

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