Evidence map›Paper›PMID 30196827›Full record

ArticleJournal of neuroimmunology2018

Lower level noise exposure that produces only TTS modulates the immune homeostasis of cochlear macrophages.

Mitchell D Frye, Celia Zhang, Bo Hua Hu

Abstract read
In one paragraph

Article in Journal of neuroimmunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.6field-weighted citation impact, top 11% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

24 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Noise-Induced Hearing Loss.Journal of clinical medicine · 2023
    Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Circulating Nestin-GFPStem cell reviews and reports · 2021
    Article
  15. Review
  16. Review
  17. Immune Response of Macrophage Population to Cochlear Implantation: Cochlea Immune Cells.Otology & neurotology : official publication of the American Otological Society, American Neurotology Society [and] European Academy of Otology and Neurotology · 2020
    Article
  18. Article
  19. Article
  20. Inflammation associated with noise-induced hearing loss.The Journal of the Acoustical Society of America · 2019
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Mitchell D FryeCenter for Hearing and Deafness, University at Buffalo, 137 Cary Hall, 3435 Main Street, Buffalo, NY 14214, USA. Electronic address: mfrye@buffalo.edu.
Celia ZhangCenter for Hearing and Deafness, University at Buffalo, 137 Cary Hall, 3435 Main Street, Buffalo, NY 14214, USA. Electronic address: celiazha@buffalo.edu.
Bo Hua HuCenter for Hearing and Deafness, University at Buffalo, 137 Cary Hall, 3435 Main Street, Buffalo, NY 14214, USA. Electronic address: bhu@buffalo.edu.
Women & Children's Hospital of Buffalo · US

Funding

Noise-induced acute hair cell DeathR01DC010154 · NIDCD · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI HU, BO HUA · 2010 to 2014
$2.0M
NIDCD NIH HHS R01 DC010154
6 · The paper itself

Abstract

Noise exposure producing temporary threshold shifts (TTS) has been demonstrated to cause permanent changes to cochlear physiology and hearing function. Several explanations have been purported to underlie these long-term changes in cochlear function, such as damage to sensory cell stereocilia and synaptic connections between sensory cells and their innervation by spiral ganglion neurons, and demyelination of the auditory nerve. Though these structural defects have been implicated in hearing difficulty, cochlear responses to this stress damage remains poorly understood. Here, we report the activation of the cochlear immune system following exposure to lower level noise (LLN) that causes only TTS. Using multiple morphological, molecular and functional parameters, we assessed the responses of macrophages, the primary immune cell population in the cochlea, to the LLN exposure. This study reveals that a LLN that causes only TTS increases the macrophage population in cochlear regions immediately adjacent to sensory cells and their innervations. Many of these cells acquire an activated morphology and express the immune molecules CCL2 and ICAM1 that are important for macrophage inflammatory activity and adhesion. However, LLN exposure reduces macrophage phagocytic ability. While the activated morphology of cochlear macrophages reverses, the complete recovery is not achieved 2 months after the LLN exposure. Taken together, these observations clearly implicate the cochlear immune system in the cochlear response to LLN that causes no permanent threshold change.

Indexed as

Acoustic StimulationAnimalsAuditory ThresholdCochleaEvoked Potentials, Auditory, Brain StemFemaleHomeostasisMacrophagesMaleMiceMice, Inbred CBANoiseCochleaImmunityInflammationLower level noiseMacrophageTemporary threshold shift

Identifiers

PMID30196827
PMCPMC6132261
OpenAlexW2810632845

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.