Department of Surgery, Stomatology, Pathology and Radiology, Bauru School of Dentistry, University of São Paulo, 17012-901 Bauru, SP, Brazil.
Department of Prosthodontics and Periodontology, Bauru School of Dentistry, University of São Paulo, 17012-901 Bauru, SP, Brazil.
Cells. 2019 Jul 12;8(7):707. doi: 10.3390/cells8070707.
The presence of in the biofilm underlying the dental prosthesis is related to denture stomatitis (DS), an inflammatory reaction of the oral mucosa. The oral epithelium, a component of the innate immune response, has the ability to react to fungal invasion. In this study, we evaluated the in vitro effect of viable on the apoptosis, nitric oxide (NO) production, and β-defensin 2 () expression and production of human palate epithelial cells (HPECs). We further determined whether or not these effects were correlated with fungal invasion of epithelial cells. Interaction between HPEC primary culture and was obtained through either direct or indirect cell-cell contact with a supernatant from a hyphal fungus. We found that the hyphae supernatants were sufficient to induce slight HPEC apoptosis, which occurred prior to the activation of the specific mechanisms of epithelial defense. The epithelial defense responses were found to occur via NO and antimicrobial peptide hBD-2 production only during direct contact between and HPECs and coincided with the fungus's intraepithelial invasion. However, although the hBD-2 levels remained constant in the HPEC supernatants over time, the NO release and gene expression were reduced at a later time (10 h), indicating that the epithelial defense capacity against the fungal invasion was not maintained in later phases. This aspect of the immune response was associated with increased epithelial invasion and apoptosis maintenance.
义齿性口炎(DS)是一种口腔黏膜炎性反应,与义齿下方生物膜中 的存在有关。口腔上皮是先天免疫反应的一个组成部分,具有对真菌感染作出反应的能力。在这项研究中,我们评估了活 的体外效应对人腭上皮细胞(HPECs)凋亡、一氧化氮(NO)产生和 β-防御素 2 () 表达和产生的影响。我们还进一步确定了这些效应是否与上皮细胞的真菌感染有关。通过真菌菌丝体上清液与 HPEC 原代培养物的直接或间接细胞-细胞接触获得 HPEC 与 的相互作用。我们发现,菌丝体上清液足以诱导 HPEC 轻微凋亡,这发生在上皮防御的特定机制激活之前。上皮防御反应仅在 和 HPECs 之间直接接触时通过 NO 和抗菌肽 hBD-2 的产生而发生,同时与真菌的上皮内入侵相一致。然而,尽管 hBD-2 水平在 HPEC 上清液中随时间的推移保持不变,但在稍后的时间点(10 小时)NO 释放和 基因表达减少,表明上皮对真菌入侵的防御能力在后期阶段无法维持。这种免疫反应的方面与上皮细胞的入侵增加和凋亡维持有关。