International immunopharmacology · 2023
Lutein attenuates Propionibacterium acnes-induced inflammation by inhibiting pyroptosis of human keratinocyte cells via TLR4/NLRP3/Caspase-1 pathway.
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Chen Yan, Yi Sha, Wang Qing, Xiong Haojun, Yuan Jingyi, Zhang Yuting, Yang Lin, Zhong Guishu, Li Xiang, Zhu Tingting
Аннотация
BACKGROUND: Previous studies found Propionibacterium acnes (P. acnes) has a strong association with acne inflammation and cell pyroptosis. Because of the various side effects of current acne medicines, it is important to explore alternative drugs with anti-inflammatory activity against P. acnes. we explored the effect of Lutein on P. acnes-induced cell pyroptosis and accelerated the recovery of acne inflammation in vitro and vivo.
METHODS: Lutein was utilized to expose HaCaT keratinocytes, then we reassessed the effect of Lutein on the cell apoptosis, pyroptotic-associated inflammatory factors and catabolic enzymes in heat-killed P. acnes-treated HaCaT cells. Next, living P. acnes was intradermally injected into the right ears of ICR mice to induce mice with acne inflammation, and the effect of Lutein on living P. acnes-induced inflammation was investigated. Moreover, we explored the mechanism of Lutein on TLR4/NLRP3/Caspase-1 pathways by ELISA, immunofluorescence microscopy, and western blot assay.
RESULTS: Heat-killed P. acnes triggered remarkable cell pyroptosis, pyroptotic inflammatory factors and catabolic enzymes in HaCaT cells, including up-regulating interleukin (IL)-1β, IL-18, TNF-α, MMP3, MMP13, ADAMTS4, and ADAMTS5, TLR4, NLRP3, caspase-1, and the ratio of gasdermin D to cleaved gasdermin D, whereas these effects were suppressed by Lutein. In addition, Lutein effectively improved ear redness, swelling, and the expression of TLR4, IL-1β and TNF-α in vivo. Finally, NLRP3 activator (nigericin) increased caspase-1, IL-1β and IL-18 level, while TLR4 inhibitor (TAK-242) significantly blocked this effect in heat-killed P. acnes-treated cells.
CONCLUSIONS: Lutein attenuated P. acnes-caused pyroptosis of HaCaTs and the subsequent acne inflammation via the TLR4/NLRP3/Caspase-1 pathway.
METHODS: Lutein was utilized to expose HaCaT keratinocytes, then we reassessed the effect of Lutein on the cell apoptosis, pyroptotic-associated inflammatory factors and catabolic enzymes in heat-killed P. acnes-treated HaCaT cells. Next, living P. acnes was intradermally injected into the right ears of ICR mice to induce mice with acne inflammation, and the effect of Lutein on living P. acnes-induced inflammation was investigated. Moreover, we explored the mechanism of Lutein on TLR4/NLRP3/Caspase-1 pathways by ELISA, immunofluorescence microscopy, and western blot assay.
RESULTS: Heat-killed P. acnes triggered remarkable cell pyroptosis, pyroptotic inflammatory factors and catabolic enzymes in HaCaT cells, including up-regulating interleukin (IL)-1β, IL-18, TNF-α, MMP3, MMP13, ADAMTS4, and ADAMTS5, TLR4, NLRP3, caspase-1, and the ratio of gasdermin D to cleaved gasdermin D, whereas these effects were suppressed by Lutein. In addition, Lutein effectively improved ear redness, swelling, and the expression of TLR4, IL-1β and TNF-α in vivo. Finally, NLRP3 activator (nigericin) increased caspase-1, IL-1β and IL-18 level, while TLR4 inhibitor (TAK-242) significantly blocked this effect in heat-killed P. acnes-treated cells.
CONCLUSIONS: Lutein attenuated P. acnes-caused pyroptosis of HaCaTs and the subsequent acne inflammation via the TLR4/NLRP3/Caspase-1 pathway.