Polyphyllin I Inhibits Propionibacterium acnes-Induced IL-8 Secretion in HaCaT Cells by Downregulating the CD36/NOX1/ROS/NLRP3/IL-1β Pathway

• Published in: Evidence-based complementary and alternative medicine Vol. 2021; pp. 1 - 11
• Main Authors: Yang, Shuyun, Jiang, Ying, Yu, Xiuqin, Zhu, Liping, Wang, Lu, Mao, Jingzhu, Wang, Miaomiao, Zhou, Naihui, Yang, Ziliang, Liu, Ying, Zhu, Tingting
• Format: Journal Article
• Language: English
• Published: New York Hindawi 2021; Hindawi Limited
• Subjects: Acne; Anti-inflammatory agents; Antibodies; Cancer therapies; Carbon dioxide; CD36 antigen; Cell proliferation; Cytokines; Drug resistance; IL-1β; Inflammasomes; Inflammation; Interleukin 8; Kinases; Leukocyte migration; Metastases; Monocytes; NAD(P)H oxidase; Pathogenesis; Propionibacterium acnes; Proteins; Pyrin protein; Reactive oxygen species; Reagents; Rhizomes; Saponins; Signal transduction; Skin diseases; Tumor necrosis factor-TNF; United States > US; China
• ISSN: 1741-427X; 1741-4288
• DOI: 10.1155/2021/1821220

Acne vulgaris (AV) is a chronic skin disease involving inflammation of the pilosebaceous units. Propionibacterium acnes (P. acnes) hypercolonization is one pathogenic factor for AV. P. acnes that triggers interleukin-1β (IL-1β) by activating the pyrin domain-containing 3 protein (NLRP3) inflammasome of the NOD-like receptor family in human monocytes. Reactive oxygen species (ROS) acts as a trigger for the production of IL-8 and activates theNLRP3 inflammasome. IL-8 promotes the metastasis and multiplication of different cancerous cells, whereas keratinocyte proliferation and migration contribute to the progression of AV. A steroidal saponin called polyphyllin I (PPI) that is extracted from Paris polyphylla’s rhizomes has anti-inflammatory properties. This study investigates the regulatory role of P. acnes in the secretion of IL-8 mediated by the CD36/NADPH oxidase 1 (NOX1)/ROS/NLRP3/IL-1β pathway and the effects of PPI on the CD36/NOX1/ROS/NLRP3/IL-1β/IL-8 pathway and human keratinocyte proliferation and migration. HaCaT cells were cultured and stimulated with 108 CFU/ml of P. acnes for 0, 6, 12, 18, 24, 30, and 36 hours. P. acnes induced IL-8 secretion from HaCaT cells via the CD36/NOX1/ROS/NLRP3/IL-1β pathway. PPI inhibited the CD36/NLRP3/NOX1/ROS/IL-8/IL-1β pathway and HaCaT cell proliferation and migration. PPI alleviates P. acnes-induced inflammatory responses and human keratinocyte proliferation and migration, implying a novel potential therapy for AV.