Evidence map›Paper›PMID 35433505›Full record

ArticleFrontiers in cellular and infection microbiology2022

Immunomodulation as a Protective Strategy in Chronic Otitis Media.

Anke Leichtle, Arwa Kurabi, David Leffers, Markus Därr, Clara Sophia Draf, Allen Frederic Ryan, Karl-Ludwig Bruchhage

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cellular and infection microbiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.8field-weighted citation impact, top 30% 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

7 citing papers in PubMed, 11 citations in OpenAlex.

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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

7 authors at 2 institutions in 2 countries.

Anke LeichtleDepartment of Otorhinolaryngology, Head and Neck Surgery, University of Lübeck, Lübeck, Germany.
Arwa KurabiDepartment of Otolaryngology, University of California, San Diego, San Diego, CA, United States.
David LeffersDepartment of Otorhinolaryngology, Head and Neck Surgery, University of Lübeck, Lübeck, Germany.
Markus DärrDepartment of Otorhinolaryngology, Head and Neck Surgery, University of Lübeck, Lübeck, Germany.
Clara Sophia DrafDepartment of Otolaryngology, University of California, San Diego, San Diego, CA, United States.
Allen Frederic RyanDepartment of Otolaryngology, University of California, San Diego, San Diego, CA, United States.
Karl-Ludwig BruchhageDepartment of Otorhinolaryngology, Head and Neck Surgery, University of Lübeck, Lübeck, Germany.
University of Lübeck · DEUniversity of California, San Diego · US

Funding

Middle ear responses in Otitis MediaR01DC000129 · NIDCD · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI RYAN, ALLEN F. · 1989 to 2021
$6.8M
Innovative therapy for diseases of the middle earR01DC012595 · NIDCD · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI RYAN, ALLEN F. · 2012 to 2023
$3.3M
NIDCD NIH HHS R01 DC000129NIDCD NIH HHS R01 DC012595
6 · The paper itself

Abstract

Introduction: Major features of the pathogenesis in otitis media, the most common disease in childhood, include hyperplasia of the middle ear mucosa and infiltration by leukocytes, both of which typically resolve upon bacterial clearance Methods: A stable otitis media model in wild-type mice and immunodeficient KO-mice, as well as human tissue samples from chronic otitis media, skin from the external auditory canal and middle ear mucosa removed from patients undergoing ear surgery, were studied. Gene and protein expression of innate immune signaling molecules were evaluated using microarray, qPCR and IHC. Results: Persistent mucosal hyperplasia of the middle ear mucosa in chronic otitis media resulted from gene and protein expression of inflammatory and apoptotic genes, including NODs, TNFα, Casp3 and cleaved Casp3. In clinical chronic middle ear samples, these molecules were modulated after a specific stimulation. They also induced a hyposensitive response after bacterial/NOD-/TLR-pathway double stimulation of HMEEC cells Conclusion: Uncontrolled middle ear mucosal hyperplasia is triggered by TLRs/NLRs immunoreceptor activation of downstream inflammatory and apoptotic molecules.

Indexed as

Otitis MediaTumor Necrosis Factor-alphaAnimalsCaspase 3HumansHyperplasiaImmunomodulationMiceMice, Inbred NODCaspase 3Tumor Necrosis Factor-alphaapoptosisimmunologyNOD-like receptorsotitis mediaTNFαTOLL-like receptors

Identifiers

PMID35433505
PMCPMC9005906
OpenAlexW4220844701

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.