Polyphyllin I Inhibits Propionibacterium acnes-Induced Inflammation In Vitro

• Published in: Inflammation Vol. 42; no. 1; pp. 35 - 44
• Main Authors: Zhu, Tingting, Wu, Wenjuan, Yang, Shuyun, Li, Donglin, Sun, Dongjie, He, Li
• Format: Journal Article
• Language: English
• Published: New York Springer US 01.02.2019; Springer Nature B.V
• Subjects: Acne; Anti-inflammatory agents; Biomedical and Life Sciences; Biomedicine; Cytokines; Extracellular signal-regulated kinase; Heat; Immunology; Inflammation; Interleukin 8; Internal Medicine; Keratinocytes; Kinases; MAP kinase; NF-κB protein; Original; Original Article; Pathology; Pharmacology/Toxicology; Phosphorylation; Propionibacterium acnes; Protein kinase; Rheumatology; TLR2 protein; Toll-like receptors; Tumor necrosis factor-TNF; Tumor necrosis factor-α; NF-κB; MAPK; polyphyllin I; TLR2; P. acnes
• ISSN: 0360-3997; 1573-2576
• DOI: 10.1007/s10753-018-0870-z

Propionibacterium acnes ( P. acnes ) has been implicated in the progression of acne inflammation. Because current acne medications have various side effects, it is necessary to explore alternative medications possessing anti-inflammatory activity against P. acnes . We investigated the inhibitory effects of polyphyllin I (PPI) on P. acnes -induced inflammation in vitro . In this study, we examined the effects of PPI on the production of inflammatory cytokines in HaCaT keratinocytes treated with heat-killed P. acnes . These treated HaCaT keratinocytes showed increased expression of Toll-like receptor 2 (TLR2) and production of inflammatory cytokines. PPI significantly suppressed the secretion of inflammatory cytokines, including interleukin (IL)-6, IL-8, and tumor necrosis factor (TNF)-α, and the expression of TLR2 in P. acnes -treated cells. Moreover, we studied the influence of PPI on the nuclear factor-κB (NF-κB) and mitogen-activated protein kinase (MAPK) signaling pathways in P. acnes -treated keratinocytes. PPI diminished the activation of NF-κB. Phosphorylated p38 levels were markedly increased after treatment with heat-killed P. acnes but were decreased after treatment with PPI, while the effect of PPI on ERK phosphorylation was not significant. Heat-killed P. acnes and PPI did not have any effect on JNK phosphorylation. Furthermore, we confirmed that NF-κB p65 inhibitor (BAY11-7082), p38 MAPK inhibitor (SB203580), and PPI blocked the expression of IL-8 in heat-killed P. acnes -treated cells. These results demonstrated that PPI has potential for development as a treatment for acne inflammation.