ABSTRACT
The pathogenesis of interstitial lung diseases can be broadly divided into inflammatory and fibrotic phases. The complexity of inflammation and fibrogenesis, coupled with ignorance of the initiating events in human interstitial lung diseases, accounts for the lack of substantial progress in developing therapeutic agents. In order to understand the sites of therapeutic intervention, it is important to briefly review the mechanisms of interstitial inflammation and excess collagen formation. Two potential sites of anti-inflammatory intervention are, first, to reduce the number of inflammatory cells such as lymphocytes and neutrophils and second, to block the effect of secreted products of inflammation. The generally poor clinical response, coupled with the frequent serious side effects, has led investigators to other approaches to suppress inflammation. Steroids, which are thought to prevent fibrosis by inhibiting inflammation, appear also to have a specific action on suppressing collagen gene expression.
