title: The anti-inflammatory effect of alloferon on UVB-induced skin inflammation through the down-regulation of pro-inflammatory cytokines.
abstract: UVB irradiation can induce biological changes in the skin, modulate immune responses and activate inflammatory reactions leading to skin damage. Alloferon, which is isolated from the blood of an experimentally infected insect, the blow fly Calliphora vicina, is known for its anti-viral and anti-tumor activities in mice model. However, the effect of alloferon against UVB irradiation and its specific mechanism are still unknown. In this study, we investigated the effect of alloferon on UVB-induced cutaneous inflammation in a human keratinocyte cell line, HaCaT. RPA and ELISA data showed that alloferon decreased the production of UVB-induced pro-inflammatory cytokines, such as IL-1α, IL-1β, IL-6 and IL-18, both on the mRNA and protein level. Western blot analysis was done to determine if alloferon regulates the MAPK signaling pathway since the MAPK signaling pathway is activated by numerous inflammatory mediators and environmental stresses including UVB irradiation. Alloferon inhibited the activation of p38 mitogen-activated protein kinase (MAPK) induced by UVB irradiation. Furthermore, the topical application of alloferon on the UVB exposed skin of hairless mice showed that alloferon treatment significantly inhibited an increase in epithelial thickness in chronic UVB-irradiated mouse skin. These findings suggest that alloferon has significant anti-inflammatory effects not only on UVB-induced inflammation in the human keratinocyte cell line, HaCaT, but also on mouse skin.
authors.affiliation: Department of Anatomy, Seoul National University College of Medicine, #103 Daehak-ro, Chongno-gu, Seoul, 110-799, Republic of Korea.
authors.forename: Yejin
authors.initials: Y
authors.lastname: Kim
authors.forename: Seung Koo
authors.initials: SK
authors.lastname: Lee
authors.forename: Seyeon
authors.initials: S
authors.lastname: Bae
authors.forename: Hyemin
authors.initials: H
authors.lastname: Kim
authors.forename: Yunseong
authors.initials: Y
authors.lastname: Park
authors.forename: Nag Kyun
authors.initials: NK
authors.lastname: Chu
authors.forename: Stephanie G
authors.initials: SG
authors.lastname: Kim
authors.forename: Hang-Rae
authors.initials: HR
authors.lastname: Kim
authors.forename: Young-Il
authors.initials: YI
authors.lastname: Hwang
authors.forename: Jae Seung
authors.initials: JS
authors.lastname: Kang
authors.forename: Wang Jae
authors.initials: WJ
authors.lastname: Lee
mesh_terms: D000818:Animals; D000970:Antineoplastic Agents / Q000494:pharmacology; D000998:Antiviral Agents / Q000494:pharmacology; D002460:Cell Line; D016207:Cytokines / Q000096:biosynthesis / Q000276:immunology*; D003872:Dermatitis / Q000188:drug therapy / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D015536:Down-Regulation / Q000187:drug effects* / Q000276:immunology / Q000528:radiation effects; D006801:Humans; D018836:Inflammation Mediators / Q000276:immunology* / Q000378:metabolism; D020935:MAP Kinase Signaling System / Q000187:drug effects / Q000276:immunology / Q000528:radiation effects; D010455:Peptides / Q000494:pharmacology*; D012333:RNA, Messenger / Q000096:biosynthesis / Q000276:immunology; D012867:Skin / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D014466:Ultraviolet Rays / Q000009:adverse effects*
chemical_list: C510535:Alloferon; D000970:Antineoplastic Agents; D000998:Antiviral Agents; D016207:Cytokines; D018836:Inflammation Mediators; D010455:Peptides; D012333:RNA, Messenger