title: Molecular profile of cochlear immunity in the resident cells of the organ of Corti.
abstract: BACKGROUND
  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.
  
  
  METHODS
  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.
  
  
  RESULTS
  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.
  
  
  CONCLUSIONS
  The cochlear resident cells in the organ of Corti have immune capacity and participate in the cochlear immune response to acoustic overstimulation.
authors.forename: Qunfeng
authors.initials: Q
authors.lastname: Cai
authors.forename: R Robert
authors.initials: RR
authors.lastname: Vethanayagam
authors.forename: Shuzhi
authors.initials: S
authors.lastname: Yang
authors.forename: Jonathan
authors.initials: J
authors.lastname: Bard
authors.forename: Jennifer
authors.initials: J
authors.lastname: Jamison
authors.forename: Daniel
authors.initials: D
authors.lastname: Cartwright
authors.forename: Youyi
authors.initials: Y
authors.lastname: Dong
authors.affiliation: Center for Hearing and Deafness, State University of New York at Buffalo, 137 Cary Hall, 3435 Main Street, Buffalo 14214, NY, USA. bhu@buffalo.edu.
authors.forename: Bo Hua
authors.initials: BH
authors.lastname: Hu
mesh_terms: D000161:Acoustic Stimulation; D000818:Animals; D019295:Computational Biology; D016207:Cytokines / Q000235:genetics / Q000378:metabolism*; D004847:Epithelial Cells / Q000378:metabolism; D016057:Evoked Potentials, Auditory, Brain Stem / Q000502:physiology; D005786:Gene Expression Regulation / Q000502:physiology*; D005838:Genotype; D006311:Hearing Disorders / Q000209:etiology / Q000473:pathology*; D051379:Mice; D008810:Mice, Inbred C57BL; D008808:Mice, Inbred CBA; D008822:Mice, Transgenic; D009622:Noise / Q000009:adverse effects; D009925:Organ of Corti / Q000473:pathology*; D011984:Sensory Receptor Cells / Q000378:metabolism*; D015398:Signal Transduction / Q000235:genetics*; D051197:Toll-Like Receptor 4 / Q000235:genetics; D051193:Toll-Like Receptors / Q000235:genetics / Q000378:metabolism*
chemical_list: D016207:Cytokines; C493487:Tlr4 protein, mouse; D051197:Toll-Like Receptor 4; D051193:Toll-Like Receptors