Chlorin e6-Mediated Photodynamic Therapy Suppresses P. acnes-Induced Inflammatory Response via NF[kappa]B and MAPKs Signaling Pathway

Photodynamic therapy (PDT), consisting of photosensitizer, light, and oxygen has been used for the treatment of various diseases including cancers, microbial infections and skin disorders. In this study, we examined the anti-inflammatory effect of chlorin e6-mediated PDT in P. acnes-infected HaCaT c...

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Bibliographic Details
Published inPloS one Vol. 12; no. 1; p. e0170599
Main Authors Wang, Yoon-Young, Ryu, A-Reum, Jin, Solee, Jeon, Yu-Mi, Lee, Mi-Young
Format Journal Article
LanguageEnglish
Published Public Library of Science 24.01.2017
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Summary:Photodynamic therapy (PDT), consisting of photosensitizer, light, and oxygen has been used for the treatment of various diseases including cancers, microbial infections and skin disorders. In this study, we examined the anti-inflammatory effect of chlorin e6-mediated PDT in P. acnes-infected HaCaT cells using photosensitizer chlorin e6 (Ce6) and halogen light. The live and heat-killed P. acnes triggered an upregulation of inflammatory molecules such as iNOS, NO, and inflammatory cytokine in HaCaT cells and mouse model. Ce6-mediated PDT notably downregulated the expression of these inflammatory molecules in vitro and in vivo. Similarly, chlorin e6-mediated PDT was capable of regulating inflammatory response in both live and heat killed S. epidermidis exposed HaCaT cells. Moreover, phosphorylation of p38, JNK, and ERK were reduced by Ce6-mediated PDT. Ce6-mediated PDT also reduced the phosphorylation of IKK[alpha]/[beta], IĸB[alpha] and NF[kappa]B p65 in P. acnes-stimulated HaCaT cells. In addition, the dramatic increase in the nuclear translocation of NF[kappa]B p65 observed upon stimulation with P. acnes was markedly impaired by Ce6-based PDT. This is the first suggestion that Ce6-mediated PDT suppresses P. acnes-induced inflammation through modulating NF[kappa]B and MAPKs signaling pathways.
ISSN:1932-6203
1932-6203
DOI:10.1371/journal.pone.0170599