Transforming Growth Factor-β Gene Transfer to the Lung Induces Myofibroblast Presence and Pulmonary Fibrosis

Many cytokines have been implicated in the initiation or propagation of fibrogenesis. In particular, the early-phase inflammatory cytokines, interleukin (IL) and tumor necrosis factor (TNF), and members of the chemokine families, including IL and monocyte chemotactic peptide (MCP-1) are known to be present in inflamed tissue, both at the beginning and at advanced stages of fibrosis. In addition, growth and differentiating factors, such as the fibroblast growth factors (FGFs), transforming growth factors (TGFs) and platelet-derived growth factors (PDGFs) are all implicated in the pathogenesis of fibrosis through their putative mode of action and demonstrated presence in fibrotic tissue. Most data implicating the various cytokines arises from studies involving immunohistochemistry or detection of gene expression within fibrotic tissue and from in vitro experiments showing activity on matrix formation by structural cells (fibroblasts, smooth-muscle cells, etc.).