Chronic inflammation is the basis of various chronic illnesses including cancer and vascular diseases. However, much has yet to be learned how inflammation becomes chronic. Prostaglandins (PGs) are well established as mediators of acute inflammation, and recent studies in experimental animals have provided evidence that they also function in transition to and maintenance of chronic inflammation. One role PGs play in such processes is amplification of cytokine signaling. As such, PGs can facilitate acquired immunity and induce long-lasting immune inflammation. PGs also contribute to chronic inflammation by making a positive feedback loop and/or by inducing chemokines and recruiting inflammatory cells to alternate active cell populations at affected sites. PGs also contribute to tissue remodeling as seen in angiogenesis and fibrosis. Although such roles of PGs should be verified in human diseases, these findings suggest that PG signaling is a promising therapeutic target of chronic inflammatory diseases.
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