Department of Oral Medicine, Nanjing Stomatological Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, China.
Jiangsu Key Laboratory of Molecular Biology for Skin Disease and STIs, Department of Mycology, Institute of Dermatology, Chinese Academy of Medical Sciences (CAMS) & Peking Union Medical College (PUMC), Nanjing, China.
Curr Mol Med. 2024;24(6):790-800. doi: 10.2174/1566524023666230612143038.
It is well recognized that both smoke and infection are crucial risk factors for oral mucosal diseases. The nucleotide-binding domain-like receptor family pyrin domain containing 3 (NLRP3) inflammasome and its downstream effectors, interleukin (IL)-1β and IL-18, are pivotal to the host defense against and other pathogens.
The present study was designed to explore the effects of cigarette smoke and on the NLRP3 inflammasome and its downstream signal pathway cell model. Oral epithelial cells (Leuk-1 cells) were exposed to cigarette smoke extract (CSE) for 3 days and/or challenged with .
Microscopically, Leuk-1 cells exerted a defense response to by markedly limiting the formation of germ tubes and microcolonies. CSE clearly eliminated the defense response of Leuk-1 cells. Functionally, CSE repressed NLRP3 inflammasome, and IL-1β and IL-18 activation induced by in Leuk-1 cells.
Our results suggested that in oral epithelial cells, the NLRP3 inflammasome might be one of the target pathways by which CSE attenuates innate immunity and leads to oral disorders.
众所周知，吸烟和感染都是口腔黏膜疾病的重要危险因素。核苷酸结合域样受体家族含pyrin 结构域蛋白 3（NLRP3）炎性小体及其下游效应物白细胞介素（IL）-1β和 IL-18 是宿主抵抗和其他病原体的关键。
本研究旨在探讨香烟烟雾和感染对 NLRP3 炎性小体及其下游信号通路细胞模型的影响。口腔上皮细胞（Leuk-1 细胞）暴露于香烟烟雾提取物（CSE）3 天，并用处理。
显微镜下，Leuk-1 细胞通过明显限制生殖管和微菌落的形成对表现出防御反应。CSE 明显消除了 Leuk-1 细胞的防御反应。功能上，CSE 抑制了 NLRP3 炎性小体，以及 CSE 抑制了 Leuk-1 细胞中诱导的 IL-1β和 IL-18 激活。
我们的结果表明，在口腔上皮细胞中，NLRP3 炎性小体可能是 CSE 减弱先天免疫并导致口腔疾病的靶途径之一。
