Dynamic interactions between lung fibroblasts and leukocytes: implications for fibrotic lung disease.

The pulmonary fibroblast within the interstitial space of the lung has assumed a vastly expanded role over the last 15 years. While this cell is still understood to supply important structural and support proteins to its environment, the fibroblast is now also viewed as an active participant in immune and inflammatory processes within the lung. This novel role for the lung fibroblast is facilitated through a number of mechanisms, including de novo expression of contractile smooth-muscle actin, adhesion molecules, and chemotactic cytokines or chemokines. Through these and possibly other processes, the lung fibroblast is able to interface uniquely with resident and infiltrating immune cells, such as macrophages and monocytes, T cells, mast cells, and eosinophils. While the precise contributions of these cell-to-cell interactions to the initiation and maintenance of diseases in the lung are unknown, modulation of these cellular events may provide an effective treatment option in many clinical pulmonary diseases.