Spiral ganglion cells and macrophages initiate neuro-inflammation and scarring following cochlear implantation

Esperanza Bas Infante, Stefania Goncalves, Michelle Adams, Christine T Dinh, Jose M. Bas, Thomas R Van De Water, Adrien Eshraghi

Research output: Contribution to journalArticle

27 Citations (Scopus)

Abstract

Conservation of a patient's residual hearing and prevention of fibrous tissue/new bone formation around an electrode array are some of the major challenges in cochlear implant (CI) surgery. Although it is well-known that fibrotic tissue formation around the electrode array can interfere with hearing performance in implanted patients, and that associated intracochlear inflammation can initiate loss of residual hearing, little is known about the molecular and cellular mechanisms that promote this response in the cochlea. In vitro studies in neonatal rats and in vivo studies in adult mice were performed to gain insight into the pro-inflammatory, proliferative, and remodeling phases of pathological wound healing that occur in the cochlea following an electrode analog insertion. Resident Schwann cells (SC), macrophages, and fibroblasts had a prominent role in the inflammatory process in the cochlea. Leukocytes were recruited to the cochlea following insertion of a nylon filament in adult mice, where contributed to the inflammatory response. The reparative stages in wound healing are characterized by persistent neuro-inflammation of spiral ganglion neurons (SGN) and expression of regenerative monocytes/macrophages in the cochlea. Accordingly, genes involved in extracellular matrix (ECM) deposition and remodeling were up-regulated in implanted cochleae. Maturation of scar tissue occurs in the remodeling phase of wound healing in the cochlea. Similar to other damaged peripheral nerves, M2 macrophages and de-differentiated SC were observed in damaged cochleae and may play a role in cell survival and axonal regeneration. In conclusion, the insertion of an electrode analog into the cochlea is associated with robust early and chronic inflammatory responses characterized by recruitment of leukocytes and expression of pro-inflammatory cytokines that promote intracochlear fibrosis and loss of the auditory hair cells (HC) and SGN important for hearing after CI surgery.

Original languageEnglish (US)
Article number303
JournalFrontiers in Cellular Neuroscience
Volume9
Issue numberAUGUST
DOIs
StatePublished - Aug 12 2015

Fingerprint

Spiral Ganglion
Cochlear Implantation
Cochlea
Cicatrix
Macrophages
Inflammation
Electrodes
Wound Healing
Hearing
Cochlear Implants
Schwann Cells
Leukocytes
Auditory Hair Cells
Neurons
Nylons
Peripheral Nerves
Hearing Loss
Osteogenesis
Extracellular Matrix
Regeneration

Keywords

  • Cochlea
  • Cochlear implant
  • Fibrosis
  • Macrophages
  • Neuro-inflammation
  • Pathology
  • Schwann cells
  • Spiral ganglion neurons

ASJC Scopus subject areas

  • Cellular and Molecular Neuroscience

Cite this

Spiral ganglion cells and macrophages initiate neuro-inflammation and scarring following cochlear implantation. / Bas Infante, Esperanza; Goncalves, Stefania; Adams, Michelle; Dinh, Christine T; Bas, Jose M.; Van De Water, Thomas R; Eshraghi, Adrien.

In: Frontiers in Cellular Neuroscience, Vol. 9, No. AUGUST, 303, 12.08.2015.

Research output: Contribution to journalArticle

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abstract = "Conservation of a patient's residual hearing and prevention of fibrous tissue/new bone formation around an electrode array are some of the major challenges in cochlear implant (CI) surgery. Although it is well-known that fibrotic tissue formation around the electrode array can interfere with hearing performance in implanted patients, and that associated intracochlear inflammation can initiate loss of residual hearing, little is known about the molecular and cellular mechanisms that promote this response in the cochlea. In vitro studies in neonatal rats and in vivo studies in adult mice were performed to gain insight into the pro-inflammatory, proliferative, and remodeling phases of pathological wound healing that occur in the cochlea following an electrode analog insertion. Resident Schwann cells (SC), macrophages, and fibroblasts had a prominent role in the inflammatory process in the cochlea. Leukocytes were recruited to the cochlea following insertion of a nylon filament in adult mice, where contributed to the inflammatory response. The reparative stages in wound healing are characterized by persistent neuro-inflammation of spiral ganglion neurons (SGN) and expression of regenerative monocytes/macrophages in the cochlea. Accordingly, genes involved in extracellular matrix (ECM) deposition and remodeling were up-regulated in implanted cochleae. Maturation of scar tissue occurs in the remodeling phase of wound healing in the cochlea. Similar to other damaged peripheral nerves, M2 macrophages and de-differentiated SC were observed in damaged cochleae and may play a role in cell survival and axonal regeneration. In conclusion, the insertion of an electrode analog into the cochlea is associated with robust early and chronic inflammatory responses characterized by recruitment of leukocytes and expression of pro-inflammatory cytokines that promote intracochlear fibrosis and loss of the auditory hair cells (HC) and SGN important for hearing after CI surgery.",
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