Evidence map›Paper›PMID 24845404›Full record

ArticleJournal of the Association for Research in Otolaryngology : JARO2014

Systemic lipopolysaccharide induces cochlear inflammation and exacerbates the synergistic ototoxicity of kanamycin and furosemide.

Keiko Hirose, Song-Zhe Li, Kevin K Ohlemiller, Richard M Ransohoff

Open access · bronzeAbstract read
In one paragraph

Article in Journal of the Association for Research in Otolaryngology : JARO, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

58 citing papers in PubMed, 85 citations in OpenAlex.

  1. Trial
  2. Pharmacologic Inhibition of JAK1/2 Potentiates Aminoglycoside-Induced Ototoxicity.Otology & neurotology : official publication of the American Otological Society, American Neurotology Society [and] European Academy of Otology and Neurotology · 2026
    Article
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  9. Review
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  13. Anti-inflammatory Therapy Protects Spiral Ganglion Neurons After Aminoglycoside Antibiotic-Induced Hair Cell Loss.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023
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  16. Review
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  19. Article
  20. Editorial: Neuroimmunology of the Inner Ear.Frontiers in neurology · 2021
    Article
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

4 authors at 2 institutions in 1 country.

Keiko HiroseDepartment of Otolaryngology, Washington University School of Medicine, 660 South Euclid Avenue, St. Louis, MO, 63110, USA, keiko_hirose@post.harvard.edu.
Song-Zhe Li
Kevin K Ohlemiller
Richard M Ransohoff
Washington University in St. Louis · USCleveland Clinic Lerner College of Medicine · US

Funding

COCHLEAR MACROPHAGES AND EPITHELIAL REPAIRR01DC011315 · NIDCD · WASHINGTON UNIVERSITY · PI HIROSE, KEIKO · 2011 to 2020
$3.5M
NIDCD NIH HHS DC011315NIDCD NIH HHS R01 DC011315
6 · The paper itself

Abstract

Aminoglycoside antibiotics are highly effective agents against gram-negative bacterial infections, but they cause adverse effects on hearing and balance dysfunction as a result of toxicity to hair cells of the cochlea and vestibular organs. While ototoxicity has been comprehensively studied, the contributions of the immune system, which controls the host response to infection, have not been studied in antibiotic ototoxicity. Recently, it has been shown that an inflammatory response is induced by hair cell injury. In this study, we found that lipopolysaccharide (LPS), an important component of bacterial endotoxin, when given in combination with kanamycin and furosemide, augmented the inflammatory response to hair cell injury and exacerbated hearing loss and hair cell injury. LPS injected into the peritoneum of experimental mice induced a brisk cochlear inflammatory response with recruitment of mononuclear phagocytes into the spiral ligament, even in the absence of ototoxic agents. While LPS alone did not affect hearing, animals that received LPS prior to ototoxic agents had worse hearing loss compared to those that did not receive LPS pretreatment. The poorer hearing outcome in LPS-treated mice did not correlate to changes in endocochlear potential. However, LPS-treated mice demonstrated an increased number of CCR2(+) inflammatory monocytes in the inner ear when compared with mice treated with ototoxic agents alone. We conclude that LPS and its associated inflammatory response are harmful to the inner ear when coupled with ototoxic medications and that the immune system may contribute to the final hearing outcome in subjects treated with ototoxic agents.

Indexed as

AnimalsAnti-Bacterial AgentsCochleaCochlear DiseasesCX3C Chemokine Receptor 1Disease Models, AnimalDrug SynergismEar, InnerEvoked Potentials, Auditory, Brain StemFurosemideHair Cells, Auditory, OuterHeterozygoteInflammationKanamycinLipopolysaccharidesMiceAnti-Bacterial AgentsCX3C Chemokine Receptor 1Cx3cr1 protein, mouseFurosemideKanamycinLipopolysaccharidesReceptors, Chemokine

Identifiers

PMID24845404
PMCPMC4141430
OpenAlexW1997408653

What OpenQuestion holds

Textmetadata
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.