Extracellular matrix deposition and granulomatous lesions are the hallmarks of a variety of diffuse interstitial lung diseases that can lead to loss of pulmonary function. Sarcoidosis is a systemic granulomatous disease which involves the lungs,
lymph
nodes, skin, central nervous system, liver and muskuloskeletal system.
Activated macrophages and monocytes express procoagulant activity which is an initiator of extrinsic coagulation cascade for fibrin formation. And activated macrophages produce cytokines which are important for chemotaxis and differentiation of
fibroblast to produce collagen and fibronectin, which in turn, stimulate monocyte/macrophage to produce interleukin-1.
To understand the role of monocyte/macrophage and collagen in the pathogenesis of pulmonary sarcoidosis, ten subjects with pulmonary sarcoidosis (stage II and III) were investigated by bronchoalveolar lavge cells and peripheral blood mononuclear
cells.
Spontaneous release of PCA and TNF-αfrom AMs were significantly higher in patients than healthy individuals (p<0.05). Collagen could stimulate PBMCs from sarcoidosis patients and healthy PBMCs and AMs to produce PCA and TNF-αbut could not
stimulate
Ams from sarcoidosis patients. This dyscoordinate stimulation of AM/PBMC in sarcodosis seems to be related with activation with pre-exposure to the millieu in the collagen-deposited interstitium of sarcoidosis.
This data demonstrated that in atage II and III sarcoidosis, PBMCs and AMs are actively produce cytokines and PCA, and collagen deposited in the sarcoidosis may play role in perpetuating the inflammatory process.
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