Abstract
Oncostatin M (OSM), as one of the gp130/IL-6 family of cytokines, interacts with receptor complexes that include the gp130 signaling molecule and OSM receptor β OSMRβ chain subunits. OSMRβ chains are expressed relatively highly across a broad array of connective tissue (CT) cells of the lung, such as fibroblasts, smooth muscle cells, and epithelial cells, thus enabling robust responses to OSM, compared to other gp130 cytokines, in the regulation of extracellular matrix (ECM) remodeling and inflammation. OSMRβ chain expression in lung monocyte/macrophage populations is low, whereas other receptor subunits, such as that for IL-6, are present, enabling responses to IL-6. OSM is produced by macrophages and neutrophils, but not CT cells, indicating a dichotomy of OSM roles in macrophage verses CT cells in lung inflammatory disease. ECM remodeling and inflammation are components of a number of chronic lung diseases that show elevated levels of OSM. OSM-induced products of CT cells, such as MCP-1, IL-6, and PGE2 can modulate macrophage function, including the expression of OSM itself, indicating feedback loops that characterize Macrophage and CT cell interaction.
Highlights
Networks of cellular interactions are governed by many factors, including cell–cell contact, the presence of mediators at sufficient concentrations, and the sufficient expression of membrane-bound receptors or soluble receptor complexes that enable cell responses.Mediators include low molecular weight endogenous compounds and their receptors to generate alterations of cell behavior
We review oncostatin M (OSM) receptor expression, regulation of the extracellular matrix, OSM regulation of lung fibroblasts, epithelial cells, smooth muscle cells, and endothelial cells, all of which contribute to structure/function of the lung as a mucosal surface interacting with the environment
OSM was initially studied as a cytokine regulating the proliferation of cancer cells, work suggesting its potential roles in inflammation was later indicated by its regulation of IL-6 [45], granulocyte-macrophage colony stimulating factor (GM-CSF) and granulocyte CSF (G-CSF) [46] in human umbilical cord endothelial cells, as well as the acute phase response in hepatocytes [47], followed by OSM regulation of chemokines in mouse systems [48]
Summary
Networks of cellular interactions are governed by many factors, including cell–cell contact, the presence of mediators (exogenous and endogenous) at sufficient concentrations, and the sufficient expression of membrane-bound receptors or soluble receptor complexes that enable cell responses. We will focus on what is known about OSM and functions in connective tissue cells and macrophages of the lung. These cells are important in the control of acute and chronic lung inflammatory diseases, and we recognize that macrophages are only one cell type amongst many immune cells involved in homeostasis and either innate or adaptive immunity and chronic disease. We review OSM receptor expression, regulation of the extracellular matrix, OSM regulation of lung fibroblasts, epithelial cells, smooth muscle cells, and endothelial cells, all of which contribute to structure/function of the lung as a mucosal surface interacting with the environment. We comment on potential sources of OSM in the lung, and its regulation in feedback loops by mediators derived from connective tissue cells
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