Role of tumor necrosis factor-α in sensorineural hearing loss after bacterial meningitis

Shervin Aminpour, Steven P. Tinling, Hilary A Brodie

Research output: Contribution to journalArticle

50 Citations (Scopus)

Abstract

Hypothesis: Blockade of tumor necrosis factor-α with tumor necrosis factor-α antibody will reduce the extent of cochlear injury and hearing loss associated with Streptococcus pneumoniae meningitis. Background: Inflammatory mediators play a significant role in the morbidity associated with bacterial meningitis, including hearing loss and labyrinthitis ossificans, Previous studies have shown the attenuation of hearing loss by the nonspecific blockade of such pathways. Methods: Fifty Mongolian gerbils were divided into four groups. Auditory brainstem response testing was conducted to measure hearing thresholds. Streptococcus pneumoniae meningitis was induced in Groups 1 and 2. Group 2 was then given a single intraperitoneal injection of tumor necrosis factor-α antibody, whereas Group 1 received phosphate-buffered saline. Uninfected animals in Groups 3 and 4 were implanted with osmotic pumps that delivered a continuous 8-day intrathecal flow of either tumor necrosis factor-α (Group 4) or phosphate-buffered saline (Group 3). After 6 weeks, auditory brainstem response testing was repeated. The cochleas were harvested and analyzed histomorphometrically. Results: Group 2 animals with Streptococcus pneumoniae meningitis that also received tumor necrosis factor-α antibody developed significantly less hearing loss than Group 1 animals with meningitis alone. The decrease in the average threshold at 4, 8, 16, and 32 kHz was 31, 30, 25, and 28 dB sound pressure level, respectively (p < 0.0092 for each). Furthermore, histomorphometric analysis showed significantly less damage to the organ of Corti, spiral ganglion, spiral ligament, and stria vascularis in Group 2. Conversely, tumor necrosis factor-α induced meningitis animals (Group 3) showed increased hearing loss compared with phosphate-buffered saline controls (Group 4), with p < 0.0001 at all frequencies. Conclusion: Tumor necrosis factor-α plays an important role in cochlear injury after bacterial meningitis. Blockade of tumor necrosis factor-α reduces postmeningitic hearing loss and cochlear injury. Induction of meningitis with intrathecal tumor necrosis factor-α also resulted in hearing loss and cochlear injury similar to bacterial meningitis.

Original languageEnglish (US)
Pages (from-to)602-609
Number of pages8
JournalOtology and Neurotology
Volume26
Issue number4
DOIs
StatePublished - Jul 2005

Fingerprint

Bacterial Meningitides
Sensorineural Hearing Loss
Tumor Necrosis Factor-alpha
Pneumococcal Meningitis
Hearing Loss
Meningitis
Brain Stem Auditory Evoked Potentials
Cochlea
Phosphates
Wounds and Injuries
Antibodies
Spiral Ligament of Cochlea
Labyrinthitis
Stria Vascularis
Spiral Ganglion
Organ of Corti
Gerbillinae
Intraperitoneal Injections
Hearing
Morbidity

Keywords

  • Disease
  • Hearing loss
  • Meningitis
  • Tumor necrosis factor-α

ASJC Scopus subject areas

  • Otorhinolaryngology
  • Neuroscience(all)

Cite this

Role of tumor necrosis factor-α in sensorineural hearing loss after bacterial meningitis. / Aminpour, Shervin; Tinling, Steven P.; Brodie, Hilary A.

In: Otology and Neurotology, Vol. 26, No. 4, 07.2005, p. 602-609.

Research output: Contribution to journalArticle

@article{3be16e13551043979fdd5df8b6927ce9,
title = "Role of tumor necrosis factor-α in sensorineural hearing loss after bacterial meningitis",
abstract = "Hypothesis: Blockade of tumor necrosis factor-α with tumor necrosis factor-α antibody will reduce the extent of cochlear injury and hearing loss associated with Streptococcus pneumoniae meningitis. Background: Inflammatory mediators play a significant role in the morbidity associated with bacterial meningitis, including hearing loss and labyrinthitis ossificans, Previous studies have shown the attenuation of hearing loss by the nonspecific blockade of such pathways. Methods: Fifty Mongolian gerbils were divided into four groups. Auditory brainstem response testing was conducted to measure hearing thresholds. Streptococcus pneumoniae meningitis was induced in Groups 1 and 2. Group 2 was then given a single intraperitoneal injection of tumor necrosis factor-α antibody, whereas Group 1 received phosphate-buffered saline. Uninfected animals in Groups 3 and 4 were implanted with osmotic pumps that delivered a continuous 8-day intrathecal flow of either tumor necrosis factor-α (Group 4) or phosphate-buffered saline (Group 3). After 6 weeks, auditory brainstem response testing was repeated. The cochleas were harvested and analyzed histomorphometrically. Results: Group 2 animals with Streptococcus pneumoniae meningitis that also received tumor necrosis factor-α antibody developed significantly less hearing loss than Group 1 animals with meningitis alone. The decrease in the average threshold at 4, 8, 16, and 32 kHz was 31, 30, 25, and 28 dB sound pressure level, respectively (p < 0.0092 for each). Furthermore, histomorphometric analysis showed significantly less damage to the organ of Corti, spiral ganglion, spiral ligament, and stria vascularis in Group 2. Conversely, tumor necrosis factor-α induced meningitis animals (Group 3) showed increased hearing loss compared with phosphate-buffered saline controls (Group 4), with p < 0.0001 at all frequencies. Conclusion: Tumor necrosis factor-α plays an important role in cochlear injury after bacterial meningitis. Blockade of tumor necrosis factor-α reduces postmeningitic hearing loss and cochlear injury. Induction of meningitis with intrathecal tumor necrosis factor-α also resulted in hearing loss and cochlear injury similar to bacterial meningitis.",
keywords = "Disease, Hearing loss, Meningitis, Tumor necrosis factor-α",
author = "Shervin Aminpour and Tinling, {Steven P.} and Brodie, {Hilary A}",
year = "2005",
month = "7",
doi = "10.1097/01.mao.0000178121.28365.0d",
language = "English (US)",
volume = "26",
pages = "602--609",
journal = "Otology and Neurotology",
issn = "1531-7129",
publisher = "Lippincott Williams and Wilkins",
number = "4",

}

TY - JOUR

T1 - Role of tumor necrosis factor-α in sensorineural hearing loss after bacterial meningitis

AU - Aminpour, Shervin

AU - Tinling, Steven P.

AU - Brodie, Hilary A

PY - 2005/7

Y1 - 2005/7

N2 - Hypothesis: Blockade of tumor necrosis factor-α with tumor necrosis factor-α antibody will reduce the extent of cochlear injury and hearing loss associated with Streptococcus pneumoniae meningitis. Background: Inflammatory mediators play a significant role in the morbidity associated with bacterial meningitis, including hearing loss and labyrinthitis ossificans, Previous studies have shown the attenuation of hearing loss by the nonspecific blockade of such pathways. Methods: Fifty Mongolian gerbils were divided into four groups. Auditory brainstem response testing was conducted to measure hearing thresholds. Streptococcus pneumoniae meningitis was induced in Groups 1 and 2. Group 2 was then given a single intraperitoneal injection of tumor necrosis factor-α antibody, whereas Group 1 received phosphate-buffered saline. Uninfected animals in Groups 3 and 4 were implanted with osmotic pumps that delivered a continuous 8-day intrathecal flow of either tumor necrosis factor-α (Group 4) or phosphate-buffered saline (Group 3). After 6 weeks, auditory brainstem response testing was repeated. The cochleas were harvested and analyzed histomorphometrically. Results: Group 2 animals with Streptococcus pneumoniae meningitis that also received tumor necrosis factor-α antibody developed significantly less hearing loss than Group 1 animals with meningitis alone. The decrease in the average threshold at 4, 8, 16, and 32 kHz was 31, 30, 25, and 28 dB sound pressure level, respectively (p < 0.0092 for each). Furthermore, histomorphometric analysis showed significantly less damage to the organ of Corti, spiral ganglion, spiral ligament, and stria vascularis in Group 2. Conversely, tumor necrosis factor-α induced meningitis animals (Group 3) showed increased hearing loss compared with phosphate-buffered saline controls (Group 4), with p < 0.0001 at all frequencies. Conclusion: Tumor necrosis factor-α plays an important role in cochlear injury after bacterial meningitis. Blockade of tumor necrosis factor-α reduces postmeningitic hearing loss and cochlear injury. Induction of meningitis with intrathecal tumor necrosis factor-α also resulted in hearing loss and cochlear injury similar to bacterial meningitis.

AB - Hypothesis: Blockade of tumor necrosis factor-α with tumor necrosis factor-α antibody will reduce the extent of cochlear injury and hearing loss associated with Streptococcus pneumoniae meningitis. Background: Inflammatory mediators play a significant role in the morbidity associated with bacterial meningitis, including hearing loss and labyrinthitis ossificans, Previous studies have shown the attenuation of hearing loss by the nonspecific blockade of such pathways. Methods: Fifty Mongolian gerbils were divided into four groups. Auditory brainstem response testing was conducted to measure hearing thresholds. Streptococcus pneumoniae meningitis was induced in Groups 1 and 2. Group 2 was then given a single intraperitoneal injection of tumor necrosis factor-α antibody, whereas Group 1 received phosphate-buffered saline. Uninfected animals in Groups 3 and 4 were implanted with osmotic pumps that delivered a continuous 8-day intrathecal flow of either tumor necrosis factor-α (Group 4) or phosphate-buffered saline (Group 3). After 6 weeks, auditory brainstem response testing was repeated. The cochleas were harvested and analyzed histomorphometrically. Results: Group 2 animals with Streptococcus pneumoniae meningitis that also received tumor necrosis factor-α antibody developed significantly less hearing loss than Group 1 animals with meningitis alone. The decrease in the average threshold at 4, 8, 16, and 32 kHz was 31, 30, 25, and 28 dB sound pressure level, respectively (p < 0.0092 for each). Furthermore, histomorphometric analysis showed significantly less damage to the organ of Corti, spiral ganglion, spiral ligament, and stria vascularis in Group 2. Conversely, tumor necrosis factor-α induced meningitis animals (Group 3) showed increased hearing loss compared with phosphate-buffered saline controls (Group 4), with p < 0.0001 at all frequencies. Conclusion: Tumor necrosis factor-α plays an important role in cochlear injury after bacterial meningitis. Blockade of tumor necrosis factor-α reduces postmeningitic hearing loss and cochlear injury. Induction of meningitis with intrathecal tumor necrosis factor-α also resulted in hearing loss and cochlear injury similar to bacterial meningitis.

KW - Disease

KW - Hearing loss

KW - Meningitis

KW - Tumor necrosis factor-α

UR - http://www.scopus.com/inward/record.url?scp=22644434475&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=22644434475&partnerID=8YFLogxK

U2 - 10.1097/01.mao.0000178121.28365.0d

DO - 10.1097/01.mao.0000178121.28365.0d

M3 - Article

VL - 26

SP - 602

EP - 609

JO - Otology and Neurotology

JF - Otology and Neurotology

SN - 1531-7129

IS - 4

ER -