Cai Qunfeng, Vethanayagam R Robert, Yang Shuzhi, Bard Jonathan, Jamison Jennifer, Cartwright Daniel, Dong Youyi, Hu Bo Hua
Center for Hearing and Deafness, State University of New York at Buffalo, 137 Cary Hall, 3435 Main Street, Buffalo 14214, NY, USA.
J Neuroinflammation. 2014 Oct 14;11:173. doi: 10.1186/s12974-014-0173-8.
The cochlea is the sensory organ of hearing. In the cochlea, the organ of Corti houses sensory cells that are susceptible to pathological insults. While the organ of Corti lacks immune cells, it does have the capacity for immune activity. We hypothesized that resident cells in the organ of Corti were responsible for the stress-induced immune response of the organ of Corti. This study profiled the molecular composition of the immune system in the organ of Corti and examined the immune response of non-immune epithelial cells to acoustic overstimulation.
Using high-throughput RNA-sequencing and qRT-PCR arrays, we identified immune- and inflammation-related genes in both the cochlear sensory epithelium and the organ of Corti. Using bioinformatics analyses, we cataloged the immune genes expressed. We then examined the response of these genes to acoustic overstimulation and determined how changes in immune gene expression were related to sensory cell damage.
The RNA-sequencing analysis reveals robust expression of immune-related genes in the cochlear sensory epithelium. The qRT-PCR array analysis confirms that many of these genes are constitutively expressed in the resident cells of the organ of Corti. Bioinformatics analyses reveal that the genes expressed are linked to the Toll-like receptor signaling pathway. We demonstrate that expression of Toll-like receptor signaling genes is predominantly from the supporting cells in the organ of Corti cells. Importantly, our data demonstrate that these Toll-like receptor pathway genes are able to respond to acoustic trauma and that their expression changes are associated with sensory cell damage.
The cochlear resident cells in the organ of Corti have immune capacity and participate in the cochlear immune response to acoustic overstimulation.
耳蜗是听觉的感觉器官。在耳蜗中,柯蒂氏器容纳着易受病理损伤的感觉细胞。虽然柯蒂氏器缺乏免疫细胞,但它确实具有免疫活性。我们推测柯蒂氏器中的驻留细胞负责柯蒂氏器的应激诱导免疫反应。本研究分析了柯蒂氏器中免疫系统的分子组成,并研究了非免疫上皮细胞对声学过度刺激的免疫反应。
使用高通量RNA测序和qRT-PCR阵列,我们在耳蜗感觉上皮和柯蒂氏器中鉴定了免疫和炎症相关基因。通过生物信息学分析,我们对表达的免疫基因进行了分类。然后,我们检查了这些基因对声学过度刺激的反应,并确定免疫基因表达的变化与感觉细胞损伤之间的关系。
RNA测序分析显示耳蜗感觉上皮中免疫相关基因的强烈表达。qRT-PCR阵列分析证实这些基因中的许多在柯蒂氏器的驻留细胞中组成性表达。生物信息学分析表明,表达的基因与Toll样受体信号通路相关。我们证明Toll样受体信号基因的表达主要来自柯蒂氏器细胞中的支持细胞。重要的是,我们的数据表明这些Toll样受体途径基因能够对声学创伤做出反应,并且它们的表达变化与感觉细胞损伤相关。
柯蒂氏器中的耳蜗驻留细胞具有免疫能力,并参与耳蜗对声学过度刺激的免疫反应。