plays a pivotal role in pulmonary fibrosis

Pulmonary fibrosis is considered a deleterious consequence of persistent lung inflammation, but the mechanism by which inflammation leads to fibrosis remains incompletely understood. In June 15 Journal of Clinical Investigation, Martin Kolb and colleagues from McMaster University, Ontario, Canada, show how acute tissue injury in the lung — initiated by a highly proinflammatory cytokine — IL-1β, converts to progressive fibrotic changes.Kolb et al. used adenoviral gene transfer to

Tudor Toma(ttoma@mail.dntis.ro)
Jun 19, 2001

Pulmonary fibrosis is considered a deleterious consequence of persistent lung inflammation, but the mechanism by which inflammation leads to fibrosis remains incompletely understood. In June 15 Journal of Clinical Investigation, Martin Kolb and colleagues from McMaster University, Ontario, Canada, show how acute tissue injury in the lung — initiated by a highly proinflammatory cytokine — IL-1β, converts to progressive fibrotic changes.

Kolb et al. used adenoviral gene transfer to transiently overexpress IL-1β in rat lungs and found an acute alveolar inflammation with subsequent induction of TGF-β expression that led to progressive interstitial fibrogenesis over the next 60 days. The sustained expression of TGF-β was associated with matrix deposition and accumulation of myofibroblasts similar to the changes seen in human pulmonary fibrosis (J Clin Invest 2001, 107:1529-1536).

These findings suggest that IL-1β plays a pivotal role in the induction of fibrosis and may be a target for...

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