Immune defense is the primary function associated with the differentially expressed genes in the cochlea following acoustic trauma

Abstract

Our previous RNA-sequencing analysis of the rat cochlear genes identified multiple biological processes and molecular pathways in the cochlear response to acoustic overstimulation. However, the biological processes and molecular pathways that are common to other species have not been documented. The identification of these common stress processes is pivotal for a better understanding of the essential response of the cochlea to acoustic injury. Here, we compared the RNA-sequencing data collected from mice and rats that sustained a similar, but not identical, acoustic injury. The transcriptome analysis of cochlear genes identified the differentially expressed genes in the mouse and rat samples. Bioinformatics analysis revealed a marked similarity in the changes in the biological processes between the two species, although the differentially expressed genes did not overlap well. The common processes associated with the differentially expressed genes are primarily associated with immunity and inflammation, which include the immune response, response to wounding, the defense response, chemotaxis and inflammatory responses. Moreover, analysis of the molecular pathways showed considerable overlap between the two species. The common pathways include cytokine-cytokine receptor interactions, the chemokine signaling pathway, the Toll-like receptor signaling pathway, and the NOD-like receptor signaling pathway. Further analysis of the transcriptional regulators revealed common upstream regulators of the differentially expressed genes, and these upstream regulators are also functionally related to the immune and inflammatory responses. These results suggest that the immune and inflammatory responses are the essential responses to acoustic overstimulation in the cochlea.

Loss of sestrin 2 potentiates the early onset of age-related sensory cell degeneration in the cochlea

“…The toxic cellular components released by dying sensory cells could cause an increased inflammatory response. This view is supported by a previous finding that SESN2 expression prevents inflammatory responses initiated by the activation of Toll-like receptors (Tlr) in macrophages (Yang et al, 2016). Tlr are a group of membrane sensor molecules that can detect both extrinsic molecules from bacteria and intrinsic molecules from damaged cells.…”

Larval Zebrafish Lateral Line as a Model for Acoustic Trauma

“…While the magnitude of protection likely depends on the precise acoustic stimulus employed and the method of Z-VAD delivery, the collective data suggest that reliance on caspase cleavage is conserved between rodent and zebrafish models of acoustic trauma. Differential gene expression patterns have also been identified in noise-exposed cochlea ( Cho et al, 2004 ; Kirkegaard et al, 2006 ; Yang et al, 2016 ). The importance of protein synthesis in acoustic trauma is difficult to test in rodents due to the high systemic toxicity of protein synthesis inhibitors ( Hoffmann et al, 2010 ).…”

Residential traffic noise exposure and vestibular schwannoma – a Danish case–control study

“…Animal studies have found that noise induces mechanical trauma to the eighth cranial nerve, and surrounding structures, including the cochlea [10,11], and it has been proposed that during repair of these damages, DNA errors could be replicated during cell division, resulting in pathological proliferation [3]. The mechanical stress has also been proposed to entail subsequent biological and molecular stress, including oxidative stress, excitotoxity, and inflammation [11]. Rodent studies examining gene expression following acoustic overstimulation suggested that the primary pathways affected were immune and inflammatory pathways [11].…”

“…The mechanical stress has also been proposed to entail subsequent biological and molecular stress, including oxidative stress, excitotoxity, and inflammation [11]. Rodent studies examining gene expression following acoustic overstimulation suggested that the primary pathways affected were immune and inflammatory pathways [11]. A study of noise exposure in zebrafish found genes involved in cell proliferation, apoptosis and immune functions to be significantly regulated in the inner ear after exposure [12].…”