title: CCL28 production in HaCaT cells was mediated by different signal pathways from CCL27.
abstract: Both CCL27 and CCL28 are ligands for CCR10 and attract CCR10(+) lymphocytes. We previously demonstrated that CCL27 and CCL28 were strongly expressed in sera and lesional keratinocytes of patients with atopic dermatitis and psoriasis vulgaris. However, the regulation of CCL27 and CCL28 production in keratinocytes has not been well documented. In this study, we showed that CCL27 and CCL28 expression and production by a human keratinocyte cell line, HaCaT cells, were strongly induced by inflammatory cytokines tumor necrosis factor-alpha and interleukin-1beta. CCL27 production was downregulated by inhibitors of p38 mitogen-activated protein kinase and nuclear factor-kappa B (NF-kappaB). By contrast, CCL28 production was downregulated by inhibitors of extracellular signal-regulated kinase and NF-kappaB. Our study results suggest that CCL28 produced by keratinocytes is mediated by different signal pathways from CCL27 and that both CCL27 and CCL28 are involved in the pathogenesis of inflammatory skin diseases.
authors.affiliation: Department of Dermatology, Faculty of Medicine, University of Tokyo, Japan. kagamis-tky@umin.ac.jp
authors.forename: Shinji
authors.initials: S
authors.lastname: Kagami
authors.forename: Hidehisa
authors.initials: H
authors.lastname: Saeki
authors.forename: Mayumi
authors.initials: M
authors.lastname: Komine
authors.forename: Takashi
authors.initials: T
authors.lastname: Kakinuma
authors.forename: Koichiro
authors.initials: K
authors.lastname: Nakamura
authors.forename: Yuichiro
authors.initials: Y
authors.lastname: Tsunemi
authors.forename: Kiyo
authors.initials: K
authors.lastname: Sasaki
authors.forename: Akihiko
authors.initials: A
authors.lastname: Asahina
authors.forename: Kunihiko
authors.initials: K
authors.lastname: Tamaki
mesh_terms: D002460:Cell Line; D054425:Chemokine CCL27; D018925:Chemokines / Q000096:biosynthesis*; D019742:Chemokines, CC / Q000378:metabolism*; D003872:Dermatitis / Q000209:etiology / Q000276:immunology / Q000378:metabolism; D006801:Humans; D007093:Imidazoles / Q000494:pharmacology; D007375:Interleukin-1 / Q000494:pharmacology; D015603:Keratinocytes / Q000187:drug effects / Q000276:immunology* / Q000378:metabolism; D008024:Ligands; D020935:MAP Kinase Signaling System / Q000187:drug effects; D016328:NF-kappa B / Q000037:antagonists & inhibitors / Q000378:metabolism; D011725:Pyridines / Q000494:pharmacology; D054447:Receptors, CCR10; D019707:Receptors, Chemokine / Q000378:metabolism; D012717:Sesquiterpenes / Q000494:pharmacology; D015398:Signal Transduction / Q000187:drug effects; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology
chemical_list: C492276:CCL27 protein, human; C414047:CCL28 protein, human; C515706:CCR10 protein, human; D054425:Chemokine CCL27; D018925:Chemokines; D019742:Chemokines, CC; D007093:Imidazoles; D007375:Interleukin-1; D008024:Ligands; D016328:NF-kappa B; D011725:Pyridines; D054447:Receptors, CCR10; D019707:Receptors, Chemokine; D012717:Sesquiterpenes; D014409:Tumor Necrosis Factor-alpha; C002669:parthenolide; C090942:4-(4-fluorophenyl)-2-(4-hydroxyphenyl)-5-(4-pyridyl)imidazole