Anti- or Pro-inflammatory?
The role of OSM as an inflammatory mediator was clear as early as 1986. Its precise effect on the immune system, as with any cytokine, is far from clear. However, two schools of thought are emerging: The first proposes that OSM is pro-inflammatory; whilst the other holds the opposite view, claiming OSM is anti-inflammatory. It is important to note that before 1997 differences in human and murine OSM receptor usage were unknown. As a result several investigators utilised human OSM in mouse assays and thus any conclusion drawn from the results of these experiments will be representative of LIF, i.e. signalling through gp130/LIFR complexes.
OSM is synthesized by stimulated T-cells and monocytes. The effects of OSM on endothelial cells suggest a pro-inflammatory role for OSM. Endothelial cells possess a large number of OSM receptors. Stimulation of a primary endothelial culture (HUVEC) with hOSM results in delayed but prolonged upregulation of P-selectin, which facilitates leukocyte adhesion and rolling, necessary for their extravasation. OSM also promotes the production of IL-6 from these cells.
As mentioned above the action of OSM as a quencher of the inflammatory response is by no means established. For example conflicting results exist as to the action of OSM on various models of arthritis. For example OSM reduces the degree of joint destruction in an antibody induced model of rheumatoid arthritis.
OSM is a major growth factor for Kaposi’s sarcoma “spindle cells”, which are of endothelial origin. These cells do not express LIFR but do express OSMR at high levels. For example OSM can modulate the expression of IL-6, an important regulator of the host defence system. OSM can regulate the expression of acute phase proteins. OSM regulates the expression of various protease and protease inhibitors, for example Gelatinase and a1-chymotrypsin inhibitor.
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