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Prostaglandins in Chronic Inflammation

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Chronic Inflammation

Abstract

Chronic inflammation underlies various chronic diseases including autoimmune diseases, cancer, neurodegenerative diseases, vascular diseases, and metabolic syndrome. Inasmuch as aspirin-like nonsteroidal anti-inflammatory drugs exert their effects by inhibiting prostaglandin (PG) biosynthesis, PGs have been traditionally thought to function only as mediators of acute inflammation by regulating short-lived events such as vasodilation, pain and fever. However, recent studies using mice deficient in PG receptor in various models of chronic inflammation have demonstrated that, in addition to their short-lived actions in acute inflammation, PGs exert long-term inflammatory actions by acting on mesenchymal, epithelial and immune cells and critically regulating gene expression at the transcription level. In these actions, PGs often cooperate with various cytokines and innate immunity molecules and amplify their actions. Through these studies, evidence now accumulates that PGs function in various aspects of chronic inflammation such as conversion to immune inflammation, amplification of inflammation by a positive feedback loop, sustained inflammatory cell infiltration, and tissue remodelling. Here we review these findings and discuss their relevance to human disease.

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Correspondence to Shuh Narumiya .

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Aoki, T., Narumiya, S. (2016). Prostaglandins in Chronic Inflammation. In: Miyasaka, M., Takatsu, K. (eds) Chronic Inflammation. Springer, Tokyo. https://doi.org/10.1007/978-4-431-56068-5_1

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