Abstract
The debate over the dual function of prostaglandins (PGs) in inflammatory conditions is continuing with unremitting vehemence1. Recent data2 indicate that a pivotal pro-inflammatory mediator role may be exerted by the cyclic endoperoxide PGG2, although PG itself is also pro-inflammatory, since it potentiates the acute inflammatory effect of other mediators3. The suggestions concerning the anti-inflammatory function of PGE were born out of in vitro studies, which have shown that PGE-mediated elevation of intracellular cyclic-AMP (cAMP) prevents the release of lysosomal enzymes from PMN leukocytes and the discharge of lymphokines from T-lymphocytes4-6. The inhibitory effect of PGE on the synthesis of collagen is another in vitro observation7 which supports a possible anti-inflammatory function. Furthermore, pharmacological doses of PGE were shown, in vivo, to inhibit granuloma formation, when applied locally into an implanted foreign body8 and to suppress the adjuvant-induced arthritis of rats9,10.
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Bonta, I.L., Parnham, M.J., Adolfs, M.J.P., van Vliet, L. (1977). Dual function of E-type prostaglandins in models of chronic inflammation. In: Willoughby, D.A., Giroud, J.P., Velo, G.P. (eds) Perspectives in Inflammation. Future Trends in Inflammation, vol 3. Springer, Dordrecht. https://doi.org/10.1007/978-94-011-7185-4_19
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DOI: https://doi.org/10.1007/978-94-011-7185-4_19
Publisher Name: Springer, Dordrecht
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