Fan Huang, Ruiqi Xie, Ruowei Li, Liu Liu, Maomao Zhao, Qiong Wang, Weida Liu, Pei Ye*, Wenmei Wang* and Xiang Wang* Pages 790 - 800 ( 11 )
<p>Background: It is well recognized that both smoke and <i>Candida</i> 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 <i>Candida</i> and other pathogens. <p> Methods: The present study was designed to explore the effects of cigarette smoke and <i>C. albicans</i> on the NLRP3 inflammasome and its downstream signal pathway <i>via in vitro</i> cell model. Oral epithelial cells (Leuk-1 cells) were exposed to cigarette smoke extract (CSE) for 3 days and/or challenged with <i>C. albicans</i>. <p> Results: Microscopically, Leuk-1 cells exerted a defense response to <i>C. albicans</i> 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 <i>C. albicans</i> in Leuk-1 cells. <p> Conclusion: 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.</p>
NLRP3 inflammasome, cigarette smoke, <i>Candida albicans</i>, oral epithelial cells, signal pathway, host defense.