Cyclooxygenase (COX)-2 is the predominant COX isoform present at sites of inflammation, and produces prostaglandins (PC) that cause swelling and pain. However, in situations where the release of protective PGs by COX-1 has been lost, the induction of COX-2 may compensate and reduce inflammatory responses. This is particularly likely in large blood vessels, where, under physiological conditions, the release of prostacyclin by COX-1, present in the endothelium, is an important component of cardiovascular homeostasis. We, and others, have recently shown that COX-2 can be induced by proinflammatory cytokines in human blood vessels, and also in human airway cells. Moreover, recent data from our group have suggested that in these structures, COX-2 is antiinflammatory at the level of cellular proliferation, adhesion receptor expression, and cytokine release.