ABSTRACT
in vitro studies investigating mononuclear cell-fibroblast interactions demonstrated that mononuclear cell cytokines present in supernatant tissue culture media of both monocytes and T lymphocytes could inhibit the proliferation and collagen synthesis of normal dermal fibroblasts. The ability of Interferons (IFN) to inhibit the activated functions of dermal fibroblasts derived from the involved skin of patients with scleroderma, morphea, or keloids has been demonstrated in several laboratories. IFNs also have been shown to modulate the in vitro metabolism of fibroblasts derived from noncutaneous sites of pathological fibrosis, including lung, synovium, penile Peyronie’s plaque, and contracted breast implant fibrous capsule. In studies of Bleomycin-Induced Murine Lung Fibrosis model, bleomycin, an antineoplastic drug, was initially administered intratracheally once to induce lung fibrosis in Swiss-Webster mice. Progressive systemic sclerosis is a disease of unknown etiology characterized by excessive deposition of connective tissue matrix components, primarily collagen, in multiple organs, including skin, heart, lung, and gastrointestinal tract, and is associated with microvascular and immunologic abnormalities.
