Prostaglandin E2 suppresses CCL27 production through EP2 and EP3 receptors in human keratinocytes Naoko Kanda, MD, PhD, Hiroshi Mitsui, MD, PhD, Shinichi.

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Presentation transcript:

Prostaglandin E2 suppresses CCL27 production through EP2 and EP3 receptors in human keratinocytes Naoko Kanda, MD, PhD, Hiroshi Mitsui, MD, PhD, Shinichi Watanabe, MD, PhD Journal of Allergy and Clinical Immunology Volume 114, Issue 6, Pages 1403-1409 (December 2004) DOI: 10.1016/j.jaci.2004.08.041 Copyright © 2004 American Academy of Allergy, Asthma and Immunology Terms and Conditions

Fig 1 Flow cytometric analysis of EP1, EP2, EP3, and EP4 expression on keratinocytes. ∗P < .05 versus EP1; †P < .05 versus EP4. MFI, Mean fluorescence intensity. Journal of Allergy and Clinical Immunology 2004 114, 1403-1409DOI: (10.1016/j.jaci.2004.08.041) Copyright © 2004 American Academy of Allergy, Asthma and Immunology Terms and Conditions

Fig 2 Inhibition by NF-κB–induced antisense oligonucleotides on TNF-α–induced CCL27 secretion (A), mRNA expression (B), and NF-κB transcriptional activity (C). ∗P < .05 versus control cells; †P < .05 versus TNF-α alone. AS, Antisense oligonucleotide; con, control; luc, luciferase. Journal of Allergy and Clinical Immunology 2004 114, 1403-1409DOI: (10.1016/j.jaci.2004.08.041) Copyright © 2004 American Academy of Allergy, Asthma and Immunology Terms and Conditions

Fig 3 Inhibition by PGE2 or EP agonists on TNF-α–induced CCL27 secretion (A), mRNA expression (B), and NF-κB transcriptional activity (C). CCL27 secretion in control cells was 0.21 ± 0.03 ng/106 cells. Fig 3, A: ∗P < .05 versus TNF-α alone. Fig 3, B and C: ∗P < .05 versus control cells; †P < 0.05 versus TNF-α alone. Journal of Allergy and Clinical Immunology 2004 114, 1403-1409DOI: (10.1016/j.jaci.2004.08.041) Copyright © 2004 American Academy of Allergy, Asthma and Immunology Terms and Conditions

Fig 4 Blocking effects of EP antagonists on PGE2-induced inhibition of CCL27 secretion (A) and NF-κB transcriptional activity (B). ∗P < .05 versus control cells; †P < .05 versus TNF-α alone; ‡P < .05 versus TNF-α plus PGE2. Journal of Allergy and Clinical Immunology 2004 114, 1403-1409DOI: (10.1016/j.jaci.2004.08.041) Copyright © 2004 American Academy of Allergy, Asthma and Immunology Terms and Conditions

Fig 5 A, PGE2-induced increase of intracellular Ca2+ concentration. B, Blocking effects of TMB-8 or U73122 on PGE2-induced inhibition of CCL27 secretion or NF-κB activity. ∗P < .05 versus control cells; †P < .05 versus TNF-α alone; ‡P < .05 versus TNF-α plus PGE2. SK&F, SK&F96365; luc, luciferase. Journal of Allergy and Clinical Immunology 2004 114, 1403-1409DOI: (10.1016/j.jaci.2004.08.041) Copyright © 2004 American Academy of Allergy, Asthma and Immunology Terms and Conditions

Fig 6 Maximal increase of intracellular Ca2+ concentration (A) and increase of intracellular cAMP level (B) by PGE2 or EP agonists (each 10 μmol/L). ∗P < .05 versus control cells. Journal of Allergy and Clinical Immunology 2004 114, 1403-1409DOI: (10.1016/j.jaci.2004.08.041) Copyright © 2004 American Academy of Allergy, Asthma and Immunology Terms and Conditions