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Proteases and emphysema.

Andrew Churg¹, Joanne L Wright

¹Department of Pathology, University of British Columbia, Vancouver, BC, Canada. achurg@interchange.ubc.ca

Current Opinion in Pulmonary Medicine

|February 9, 2005

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The protease-antiprotease theory of emphysema is complex, involving interactions between various proteases and inflammatory cells. Animal models suggest antiproteolytic therapy can help treat cigarette smoke-induced emphysema.

Area of Science:

Pulmonary Medicine
Cell Biology
Biochemistry

Background:

The protease-antiprotease theory of emphysema is widely accepted.
Identifying specific cells and proteases involved in emphysema pathogenesis remains controversial.

Purpose of the Study:

To review the current understanding of the cellular and molecular mechanisms underlying emphysema.
To explore the roles of various proteases and inflammatory mediators in emphysema development.

Main Methods:

Review of human studies and laboratory animal models of emphysema.
Analysis of protease activity (metalloproteinases, serine elastases) and inflammatory mediator signaling (TNF-alpha, IL-13).
Investigation of genetic modifications and their impact on emphysema development.

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Main Results:

Human studies show increased metalloproteinase activity in emphysema.
Animal models highlight the crucial role of neutrophils and matrix metalloproteinase-12 (MMP12) in driving emphysema.
Interference with neutrophil elastase and tumor necrosis factor-alpha signaling offers protection; metalloproteinase inhibitors may provide greater benefit.
Genetic models demonstrate emphysema induction via mediators like tumor necrosis factor-alpha, with evidence of multiple protease attacks and collagen breakdown.

Conclusions:

Emphysema pathogenesis likely involves complex interactions among multiple proteases and inflammatory mediators, not a single agent.
Relevance of animal models to human emphysema requires careful consideration due to potential discrepancies in protease roles.
Antiproteolytic therapy shows promise in ameliorating cigarette smoke-induced emphysema based on animal model evidence.