PubMed · 7254011
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A Fleming, J V Bertouch. 1981-05-16. Local injection techniques.. https://doi.org/10.5694/j.1326-5377.1981.tb135775.x
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Glucocorticosteroids (GCS) are potent anti-inflammatory and immunosuppressive agents widely used in the treatment of many medical conditions, but their mechanism of action is not yet fully understood. Some of the anti-inflammatory effects of GCS have been attributed to the synthesis of lipocortins, whereas the immunosuppressive effects are thought to be mediated through the inhibition of several immune functions through a down-regulation of cytokine gene expression. Another important mechanism of action of GCS may relate to their ability to interfere with the phenomena of adhesion and migration of inflammatory cells. In this study, the direct effects of GCS on lymphocyte adhesion capacity in vitro were investigated. We demonstrate that GCS inhibit lymphocyte adhesion to endothelium through the down-modulation of lymphocyte adhesion molecules. We also provide evidence that GCS inhibit cell aggregate formation induced by TCR ligation, which directly correlates with the down-modulation of LFA-1 and CD2, but not LFA-3 or ICAM-1. Such down-modulation was paralleled by a decrease in the steady state mRNA level of LFA-1 and CD2 gene products, which suggests a direct GCS control of the expression of these genes. Finally, we show that GCS effects are mediated through the GCS receptor, since they can be completely reversed by the GCS-R antagonist RU-486. This study supports the concept that some of the immunosuppressive and anti-inflammatory effects of GCS are likely to be exerted by the inhibition of adhesion-dependent lymphocyte functions.
Nonsteroidal anti-inflammatory (NSAID) drugs have been used to treat osteoarthritis ever since 1899, when the effects of aspirin were first recognized. Widespread use of these compounds continues despite their recognized potential toxicity, mostly because they are generally effective for palliation of the pain associated with osteoarthritis. The discovery of cyclooxygenase (COX)-1 and COX-2 has sparked interest in development of NSAID that specifically target COX-2, with the hope that such compounds would be associated with a lower incidence of adverse gastrointestinal effects. Other potential methods of avoiding adverse gastrointestinal effects associated with NSAID use include concurrent administration of prostaglandins and use of pure analgesics, such as acetaminophen. The role of nitric oxide in inflammation is an exciting area of research, and addition of nitric oxide-producing moieties to NSAID may prove to be another mechanism of avoiding gastrointestinal toxicity. There is likely to be considerable reward for the development of an NSAID that relieves pain associated with a wide variety of conditions, does not cause gastrointestinal toxicoses, and spares normal cartilage. Whether such a drug exists remains speculative.