Polyphyllin I Inhibits Propionibacterium 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-killedP. 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 inP. 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 inP. acnes-treated keratinocytes. PPI diminished the activation of NF- κB. Phosphorylated p38 levels were markedly increased after treatment with heat-killedP. acnes but were decreased after treatment with PPI, while the effect of PPI on ERK phosphorylation was not significant. Heat-killedP. 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-killedP. acnes-treated cells. These results demonstrated that PPI has potential for development as a treatment for acne inflammation.
Source: Inflammation - Category: Allergy & Immunology Source Type: research