Department of Otolaryngology Aichi Medical University School of Medicine, Aichi, Japan.
Innate Immun. 2013;19(2):115-20. doi: 10.1177/1753425912450347. Epub 2012 Jun 25.
The NO productivity of auditory cells in response to LPS was examined by using conditionally immortalized murine HEI-OC1 auditory cells. HEI-OC1 cells produced NO in response to LPS ranging from 0.1 µg/ml to 100 µg/ml in a concentration-dependent manner. LPS at 100 µg/ml exhibited no cytotoxic action against HEI-OC1 cells and led to the highest level of NO production. The NO output in LPS-treated HEI-OC1 cells gradually increased up to 72 h. LPS-induced NO production was mediated by the expression of an inducible NO synthase (iNOS) protein. TLR4 and CD14 was expressed on the cell surface of HEI-OC1 cells. LPS augmented the production of IFN-β in the MyD88-independent pathway of LPS signalling. HEI-OC1 cells produced NO in response to a TLR2 ligand but not TLR3 ligand. LPS was suggested to lead to NO production in auditory cells via iNOS expression. The immunological significance of NO production in auditory cells is discussed.
我们使用条件永生化的小鼠 HEI-OC1 听觉细胞来检测 LPS 对听觉细胞中 NO 产物的影响。HEI-OC1 细胞以浓度依赖的方式对 LPS （浓度范围为 0.1μg/ml 至 100μg/ml）产生 NO。100μg/ml 的 LPS 对 HEI-OC1 细胞没有细胞毒性作用，并导致产生最高水平的 NO。在 LPS 处理的 HEI-OC1 细胞中，NO 的输出逐渐增加至 72 小时。LPS 诱导的 NO 产生是由诱导型一氧化氮合酶（iNOS）蛋白的表达介导的。TLR4 和 CD14 表达在 HEI-OC1 细胞的细胞表面。LPS 增强了 LPS 信号通路中 MyD88 非依赖性途径中 IFN-β的产生。HEI-OC1 细胞对 TLR2 配体产生 NO，但对 TLR3 配体不产生。LPS 可能通过 iNOS 表达导致听觉细胞中产生 NO。讨论了听觉细胞中 NO 产生的免疫学意义。
