Gingival epithelium is the primary barrier against microorganism invasion and produces inflammatory cytokines. Amphotericin B, a major antifungal drug, binds to cholesterol in the mammalian cell membrane in addition to fungal ergosterol. Amphotericin B has been shown to regulate inflammatory cytokines in host cells. To investigate the suppressive effect of amphotericin B on the gingival epithelium, we examined the expression of interleukin (IL)-8 and IL-6 and involvement of MAP kinase in human gingival epithelial cells (HGEC) stimulated by Aggregatibacter actinomycetemcomitans. Amphotericin B and the p38 MAP kinase inhibitor down-regulated the A. actinomycetemcomitans-induced increase in the expression of IL-8 and IL-6 at the mRNA. The ERK inhibitor suppressed the A. actinomycetemcomitans-induced IL-8 mRNA expression. Amphotericin B inhibited the A. actinomycetemcomitans-induced phosphorylation of ERK and p38 MAP kinase. Furthermore, amphotericin B inhibited the A. actinomycetemcomitans-induced production of prostaglandin E2. These results suggest that amphotericin B regulate inflammatory responses in HGEC.

中文翻译：

---

两性霉素B下调人牙龈上皮细胞中放线杆菌聚合酶诱导的IL-8和IL-6的产生。

牙龈上皮是抵抗微生物入侵的主要屏障，并产生炎性细胞因子。两性霉素B是一种主要的抗真菌药物，除真菌麦角固醇外，还与哺乳动物细胞膜中的胆固醇结合。已经证明两性霉素B调节宿主细胞中的炎性细胞因子。为了研究两性霉素B对牙龈上皮的抑制作用，我们检查了由聚合放线菌引起的人牙龈上皮细胞（HGEC）中白介素（IL）-8和IL-6的表达以及MAP激酶的参与。两性霉素B和p38 MAP激酶抑制剂下调放线放线杆菌诱导的mRNA上IL-8和IL-6表达的增加。ERK抑制剂抑制了放线放线杆菌诱导的IL-8 mRNA表达。两性霉素B抑制了放线杆菌引起的ERK和p38 MAP激酶的磷酸化。此外，两性霉素B抑制了放线杆菌引起的前列腺素E2的产生。这些结果表明，两性霉素B调节HGEC中的炎症反应。