Fibroblasts pulmonary

Con A Concanavalin A COPD Chronic obstructive pulmonary disease COS Fibroblast-like kidney cell line established from simian cells CoVF Cobra venom CP Creatine phosphate Cp Caeruloplasmin c.p.m. Counts per minute CPJ Cartilage/pannus junction Cr The chemical symbol fir chromium CR Complement receptor CRl, CR2 CR4 Complement receptor types 1, 2 and 4 CR3-a Complement receptor type 3-[Pg.281]

Hogaboam CM, Bone-Larson CL, Lipinski S, et al. Differential monocyte chemoattractant protein-1 and chemokine receptor 2 expression by murine lung fibroblasts derived from Thl- and Th2-type pulmonary granuloma models. J Immunol 1999 163(4) 2193-2201. 

Pulmonary arterial effects. Cigarette smoke, administered to 2- and 3-month-old rats at a dose of one cigarette 10 times a day, increased significantly the volume fractions of the fibroblasts, the collagenous bundles, and the elastic laminae of the pulmonary arteries. The volume fractions of smooth muscle cells and the remainder were decreased significantly in both groups compared to controls. An increase in the stiffness of the pulmonary arteries was found in both the 2- and 3-month smoke-exposed rats . ... 

Serotonin (5-HT) produces a rapid elevation of superoxide that stimulates the mitogenesis of bovine pulmonary artery smooth muscle cells (SMCs). EGb scavenges superoxide elevated by 5-HT, hence preventing 5-HT-induced mitogenesis on both SMCs and Chinese hamster lung fibroblasts. These results indicate that EGb inhibits the cellular transduction signaling process that leads to mitogenesis, as a result of its antioxidant activity [141]. 

Breen EC. Mechanical strain increases type I collagen expression in pulmonary fibroblasts in vitro. J Appl Physiol. 2000 88 203-209. 

Adamson lYR, Bowden DH. 1990. Pulmonary reaction to long and short asbestos fibers is independent of fibroblast growth factor production by alveolar macrophages. Am J Pathol 137 523-529... 

The adverse effects of high-dose oxygen on the lungs take the form of an initial exudation of blood and fibrinous fluid into the alveoli followed by proliferation of fibroblasts and alveolar cells (2). The proliferative phase can be permanent (3). It is reflected in a reduced vital capacity and a reduced diffusion capacity (4) and appears to be proportional to the units of pulmonary toxic dose (UPTD) administered 1 UPTD is equivalent to 1 absolute atmosphere x 1 minute of exposure. If exposure exceeds 1000 UPTD it can be difficult to predict the outcome (5), owing to inter-patient differences in susceptibility. 

Khalil, N., Bareznay, O., Sporn, M. and Greenberg, A.H. (1989). Macrophage production of transforming growth fiictor beta and fibroblast collsgen synthesis in chronic pulmonary inflammation. J. Exp. Med. 170, 727-737. 

Nakamura etal., 1991 Cromwell et al. Kwon et al., 1993) and fibroblasts (Rolff etal., 1991) in response to a wide variety of pro-inflammatory stimuli such as exposure to IL-1, TNF and endotoxin. IL-8 is a chemoattractant for neutrophils, and causes degranulation of neutrophil-specific granules. It enhances the adherence of neutrophils to endothelial cells and the subendotheUal matrix (Rot, 1992). Under certain experimental conditions, IL-8 has been reported to be chemotactic for T cells and eosinophils (Taub and Oppenheim, 1993). IL-8 expression has been shown to be increased in lung tissue of patients with pulmonary fibrosis (Carr6 etal., 1991). 

Pulmonary fibroblast expression of interleukin-8 a model for alveolar macrophs -derived cytokine networking. Am. J. Respir. Cell. Mol. Biol. 5, 493-501. 

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