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The anti-inflammatory effect of alloferon on UVB-induced skin inflammation through the down-regulation of pro-inflammatory cytokines

Cited 32 time in Web of Science Cited 31 time in Scopus
Authors

Kim, Yejin; Lee, Seung Koo; Bae, Seyeon; Kim, Hyemin; Park, Yunseong; Chu, Nag Kyun; Kim, Stephanie G.; Kim, Hang-Rae; Hwang, Young-il; Kang, Jae Seung; Lee, Wang Jae

Issue Date
2013-01
Publisher
Elsevier BV
Citation
Immunology Letters, Vol.149 No.1-2, pp.110-118
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-1 alpha, IL-1 beta, 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. (C) 2012 Elsevier B.V. All rights reserved.
ISSN
0165-2478
URI
https://hdl.handle.net/10371/202657
DOI
https://doi.org/10.1016/j.imlet.2012.09.005
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Research Area Function, Immune modulation by metabolites, T-cell anergy, differentiation of memory CD8+ T cells, metabolism

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