Abstract
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.
Highlights
Acne vulgaris is a common skin disease estimated to affect 660 million people in the world, making it the 8th most common disease worldwide (2013), affecting the quality of life in those with severe cases [1,2]
The result indicated that live P. acnes induced an inflammatory response via enhancing iNOS level, but chlorin e6 (Ce6)-mediated Photodynamic therapy (PDT) inhibited the expression of iNOS
Nitrite level in the culture medium was monitored by Griess reagent assay in cells stimulated with live P. acnes with or without the application of Ce6-mediated PDT
Summary
Acne vulgaris is a common skin disease estimated to affect 660 million people in the world, making it the 8th most common disease worldwide (2013), affecting the quality of life in those with severe cases [1,2]. Acne-related skin inflammation is mediated by Propionibacterium acnes (P. acnes)’ ability of activating a class of immune system and changing the sebum’s lipid composition. The inflammatory cascade triggered by P. acnes leads to the formation of inflammatory lesions and scar formation [3,4]. Inflammation is a complex protective response against various harmful stimuli including pathogens and irritants. To abrogate the detrimental effects of inflammation, many researches.
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