Chlorin e6-Mediated Photodynamic Therapy Suppresses P. acnes-Induced Inflammatory Response via NFκB and MAPKs Signaling Pathway.
Chlorin e6-Mediated Photodynamic Therapy Suppresses P. acnes-Induced Inflammatory Response via NFκB and MAPKs Signaling Pathway.
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氯素E6介导的光动力疗法通过NFκB和MAPKS信号通路抑制了痤疮P.痤疮诱导的炎症反应。
DOI：
10.1371/journal.pone.0170599
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发表时间：
2017
期刊：
影响因子：
3.7
通讯作者：
Lee MY
中科院分区：
文献类型：
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作者：
Wang YY;Ryu AR;Jin S;Jeon YM;Lee MY
由光敏剂、光和氧气组成的光动力疗法（PDT）已用于治疗各种疾病，包括癌症、微生物感染和皮肤病。在这项研究中，我们使用光敏剂二氢卟酚e6（Ce 6）和卤素灯检测了二氢卟酚e6介导的PDT在痤疮丙酸杆菌感染的HaCaT细胞中的抗炎作用。在HaCaT细胞和小鼠模型中，活的和热灭活的痤疮丙酸杆菌引发炎症分子如iNOS、NO和炎症细胞因子的上调。Ce 6介导的PDT在体外和体内显著下调这些炎症分子的表达。类似地，二氢卟酚e6介导的PDT能够调节活的和热杀死的S.表皮暴露HaCaT细胞。此外，p38，JNK和ERK的磷酸化被Ce 6介导的PDT减少。Ce 6介导的PDT还降低了痤疮丙酸杆菌刺激的HaCaT细胞中IKKα/β、I κ B B α和NFκB B p65的磷酸化。此外，在用痤疮丙酸杆菌刺激后观察到的NFκB p65核转位的显著增加被基于Ce 6的PDT显著削弱。这首次提示Ce 6介导的PDT通过调节NFκB和MAPK信号通路抑制痤疮丙酸杆菌诱导的炎症。
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 IKKα/β, IĸBα and NFκB p65 in P. acnes-stimulated HaCaT cells. In addition, the dramatic increase in the nuclear translocation of NFκB 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 NFκB and MAPKs signaling pathways.