Maltol, a compound in Korean Red Ginseng, attenuates the Staphylococcus aureus–induced inflammasome activation in the skin

• Published in: Journal of ginseng research Vol. 48; no. 6; pp. 609 - 615
• Main Authors: Ahn, Huijeong, Yu, Sangjung, Han, Byung-Cheol, Ro, Younghye, Kim, Yo-Han, Kizaki, Keiichiro, Lee, Eunsong, Lee, Seung-Ho, Lee, Geun-Shik
• Format: Journal Article
• Language: English
• Published: Elsevier B.V 01-11-2024
• Subjects: HaCaT; Inflammasome; Keratinocytes; Korean red ginseng extract; Maltol; Keratinocytes; Korean red ginseng extract; Inflammasome; HaCaT; Maltol
• ISSN: 1226-8453
• DOI: 10.1016/j.jgr.2024.09.008

Staphylococcus aureus can cause local or systemic infections as an opportunistic pathogen and induce the activation of inflammasomes, leading to the secretion of interleukin (IL)-1β. Since S. aureus is part of the normal flora, it is essential to control it using safe, non-antibiotic substances like Korean Red Ginseng Extract (RGE). This study investigated the effects of maltol, a non-saponin compound found in RGE, on S. aureus-mediated inflammasome signaling.
Human keratinocytes (HaCaT) and macrophages were infected with S. aureus and treated with RGE and maltol. The secretion of IL-1β, an indicator of inflammasome activation, was analyzed. For the mechanistic studies, the HaCaT cells were infected with S. aureus in the presence of maltol or inflammasome inhibitors, and the generation of mitochondrial reactive oxygen species (mitROS) and IL-1β production were measured. The effect of maltol was also evaluated in S. aureus-injected mice.
RGE and maltol inhibited S. aureus-mediated IL-1β secretion in HaCaT, but not in macrophages. In the mechanistic studies, maltol suppressed the production of mitROS and the priming step of inflammasome signaling resulting in attenuated S. aureus-mediated inflammasome activation in HaCaT. In mice, maltol inhibited the production of peritoneal IL-1β and IL-6 in response to the S. aureus injection.
Maltol selectively regulated skin inflammasome activation by inhibiting mitROS generation and the inflammasome priming step.
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