Drugs, inflammation and cell adhesion receptors
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abstract
The cell adhesion receptors that participate in the extravasation and migration of leucocytes towards inflammatory foci mainly include the selectins and different members of the integrin and immunoglobulin superfamilies. These adhesion receptors mediate the sequential steps of leucocyte-endothelial cell interaction and, together with chemoattractant molecules (e.g., chemokines), direct the influx of inflammatory cells and define the characteristics of the cell infiltrate. Many different drugs, including non-steroidal anti-inflammatory drugs (NSAIDs), glucocorticoids, rheumatoid arthritis disease-modifying agents and phosphodiesterase inhibitors, interfere with the expression and/or function of cell adhesion receptors and this effect accounts for, at least in part, their anti-inflammatory activity. In recent years, novel approaches for the modulation of the cell membrane receptors involved in inflammation have been active areas in pharmaceutical research. Upgraded synthetic blocking compounds, chimeric monoclonal antibodies or improved antisense oligonucleotides represent important advances in this field. The proper development of these novel approaches, as well as other alternative strategies, will allow a better and more specific pharmacological modulation of the inflammatory phenomenon.
