Phospholipase A2 activation is the pivotal step in the effector pathway of inflammation.

Our understanding of the mechanisms of initiation and propagation of local and systemic inflammatory processes is clearly imperfect if one uses the available therapeutic modalities as a yardstick. While glucocorticoids are potent anti-inflammatory drugs, the pharmacologic target of this class of agents has not been identified with certainty, and the use of steroids is fraught with the risk of considerable and potentially dangerous side effects. On the other hand, non-steroidal anti-inflammatory drugs (NSAIDS), while more specific, are relatively weak anti-inflammatory compounds and frequently require the addition of more potent agents. Cytotoxic drugs or anti-metabolites effectively suppress acute and chronic inflammatory reactions, but also predispose to infection and initiate the development of neoplasms following long-term exposure. The inadequacy and relative non-specificity of these approaches underscore the deficiencies in our understanding of the principles that govern these responses. A better understanding of these processes will be applicable to broad categories of human disease including autoimmunity, the collagen vascular diseases, aberrations in host defense and the response to trauma and infection.