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In mice, eosinopoiesis is suppressed in vitro by prostaglandin E2 (PGE2) and in vivo by diethylcarbamazine, through a proapoptotic mechanism sequentially requiring inducible NO synthase (iNOS) and the ligand for death receptor CD95 (CD95L). We examined the roles of iNOS, cAMP\u2010mediated signaling, caspases, and CD95L\/CD95 in suppression of eosinopoiesis by PGE2 and other agents signaling through cAMP. Bone\u2010marrow collected from BALB\/c mice, or from iNOS\u2010, CD95\u2010, or CD95L\u2010deficient mutants (and wild\u2010type controls), was cultured with interleukin\u20105 (IL\u20105), alone or associated with PGE2, cAMP\u2010inducing\/mimetic agents, caspase inhibitor zVAD\u2010fmk, iNOS inhibitor aminoguanidine, or combinations thereof, and eosinopoiesis was evaluated at various times. PGE2, added up to 24 hours of culture, dose\u2010dependently suppressed eosinopoiesis, by inducing apoptosis. This effect was (a) paralleled by induction of iNOS in eosinophils; (b) duplicated by sodium nitroprusside, isoproterenol, and cAMP\u2010inducing\/mimetic agents; (c) prevented by protein kinase A inhibition. NO was produced through iNOS by dibutyryl\u2010cAMP\u2010stimulated bone\u2010marrow. Overall, PGE2 and isoproterenol shared a requirement for four effector elements (iNOS, CD95L, CD95, and terminal caspases), which together define a pathway targeted by several soluble up\u2010 and downmodulators of eosinopoiesis, including drugs, mediators of inflammation, and cytokines.<\/jats:p>","DOI":"10.1155\/2013\/208705","type":"journal-article","created":{"date-parts":[[2013,11,24]],"date-time":"2013-11-24T21:01:01Z","timestamp":1385326861000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":7,"title":["Essential Roles of PKA, iNOS, CD95\/CD95L, and Terminal Caspases in Suppression of Eosinopoiesis by PGE2 and Other cAMP\u2010Elevating Agents"],"prefix":"10.1155","volume":"2013","author":[{"given":"Bianca","family":"de 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