Evidence map›Paper›PMID 32702135›Full record

ArticleImmunology2020

Transient tear hyperosmolarity disrupts the neuroimmune homeostasis of the ocular surface and facilitates dry eye onset.

Mauricio Guzmán, Maximiliano Miglio, Irene Keitelman, Carolina Maiumi Shiromizu, Florencia Sabbione, Federico Fuentes, Analía S Trevani, Mirta N Giordano, Jeremías G Galletti

Open access · bronzeAbstract read
In one paragraph

Article in Immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed, 1 pooled it
6.5field-weighted citation impact, top 3% 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

44 citing papers in PubMed, 1 synthesis or guideline pooled it, 67 citations in OpenAlex.

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  15. CD4Proceedings of the National Academy of Sciences of the United States of America · 2024
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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

9 authors at 1 institution in 1 country.

Mauricio GuzmánLaboratorio de Inmunidad Innata, Instituto de Medicina Experimental, Academia Nacional de Medicina/CONICET, Buenos Aires, Argentina.
Maximiliano MiglioLaboratorio de Inmunidad Innata, Instituto de Medicina Experimental, Academia Nacional de Medicina/CONICET, Buenos Aires, Argentina.
Irene KeitelmanLaboratorio de Inmunidad Innata, Instituto de Medicina Experimental, Academia Nacional de Medicina/CONICET, Buenos Aires, Argentina.
Carolina Maiumi ShiromizuLaboratorio de Inmunidad Innata, Instituto de Medicina Experimental, Academia Nacional de Medicina/CONICET, Buenos Aires, Argentina.
Florencia SabbioneLaboratorio de Inmunidad Innata, Instituto de Medicina Experimental, Academia Nacional de Medicina/CONICET, Buenos Aires, Argentina.
Federico FuentesLaboratorio de Inmunidad Innata, Instituto de Medicina Experimental, Academia Nacional de Medicina/CONICET, Buenos Aires, Argentina.
Analía S TrevaniLaboratorio de Inmunidad Innata, Instituto de Medicina Experimental, Academia Nacional de Medicina/CONICET, Buenos Aires, Argentina.
Mirta N GiordanoLaboratorio de Inmunidad Innata, Instituto de Medicina Experimental, Academia Nacional de Medicina/CONICET, Buenos Aires, Argentina.
Jeremías G GallettiLaboratorio de Inmunidad Innata, Instituto de Medicina Experimental, Academia Nacional de Medicina/CONICET, Buenos Aires, Argentina.ORCID 0000-0002-5118-2540
Academia Nacional de Medicina · AR

Funding

Association for Research in Vision and Ophthalmology Roche Collaborative Research Fellowship 2018Fondo para la Investigación Científica y Tecnológica PICT 2013-1436Fondo para la Investigación Científica y Tecnológica PICT 2015-0971Fondo para la Investigación Científica y Tecnológica PICT 2018-02911
6 · The paper itself

Abstract

Dry eye disease (DED) is a highly prevalent ocular surface disorder with neuroimmune pathophysiology. Tear hyperosmolarity (THO), a frequent finding in affected patients, is considered a key element in DED pathogenesis, yet existing animal models are based on subjecting the ocular surface to the more complex desiccating stress - decreased tear production and/or increased evaporation - instead of strict hyperosmolar stress. Here we characterized a murine model of THO that does not involve desiccating stress, thus allowing us to dissect the contribution of THO to DED. Our results showed that THO is sufficient to disrupt neuroimmune homeostasis of the ocular surface in mice, and thus reproduce many sub-clinical DED findings. THO activated nuclear factor-κB signalling in conjunctival epithelial cells and increased dendritic cell recruitment and maturation, leading to more activated (CD69

Indexed as

Ocular Physiological PhenomenaAdoptive TransferAnimalsCD4-Positive T-LymphocytesCells, CulturedDry Eye SyndromesEyeHomeostasisHumansLymphocyte ActivationMiceMice, Inbred C57BLNeuroimmunomodulationNF-kappa BOsmolar ConcentrationSignal TransductionNF-kappa BTRPV1 protein, mouseTRPV Cation Channelsdry eyehyperosmolar stressocular mucosal tolerancetear hyperosmolaritytransient receptor potential vanilloid 1

Identifiers

PMID32702135
PMCPMC7496787
OpenAlexW3044238104

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.