지원사업
학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
커뮤니티
연구자들이 자신의 연구와 전문성을 널리 알리고, 새로운 협력의 기회를 만들 수 있는 네트워킹 공간이에요.
논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2024.11
- 수록면
- 609 - 615 (7page)
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초록· 키워드
오류제보하기
Background: 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.
Methods: 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.
Results: 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.
Conclusion: Maltol selectively regulated skin inflammasome activation by inhibiting mitROS generation and the inflammasome priming step.
Methods: 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.
Results: 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.
Conclusion: Maltol selectively regulated skin inflammasome activation by inhibiting mitROS generation and the inflammasome priming step.
목차
ABSTRACT
1. Introduction
2. Materials and methods
3. Results
4. Discussion
5. Conclusion
References
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