Prostaglandins and lymphokines in inflammation

It is suggested that the inflammatory process in rheumatoid arthritis (RA) results from activation of small lymphocytes to produce lymphokines, whose biological properties are appropriate to a mediator of chronic inflammation. Since prostaglandins (PGs) and allied products of arachidonic acid metabolism have properties pertinent to chronic inflammation, these compounds can also be regarded as potential mediators of chronic inflammation, a viewpoint supported by the capacity of steroids and non-steroidal anti-inflammatory drugs (NSAIDs) to suppress PG formation. Certain observations are inconsistent with PGs fulfilling this role. These anomalies may be resolved by considering PGE2 formation by macrophages to be a device for regulating lymphocyte activation. A defect of lymphocyte reactivity to PGE2 provides a basis for chronicity and has been demonstrated in multiple sclerosis (MS). Alternatively, should lymphocytes in lesions of RA be susceptible to PGE2 inhibition, one consequence of NSAID treatment may be exacerbation of joint destruction.