Evidence map›Paper›PMID 24453426›Full record

ArticleMediators of inflammation2013

Modulation of conjunctival goblet cell function by inflammatory cytokines.

L Contreras-Ruiz, A Ghosh-Mitra, M A Shatos, D A Dartt, S Masli

Open access · goldAbstract read
In one paragraph

Article in Mediators of inflammation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
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

62 citing papers in PubMed, 105 citations in OpenAlex.

  1. Trial
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  6. Ocular Surface Microbiota Alterations Following FS-LASIK and Their Association With Postoperative Dry Eye.The Canadian journal of infectious diseases & medical microbiology = Journal canadien des maladies infectieuses et de la microbiologie medicale · 2026
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  18. Resolvin D2 uses multiple CaJournal of cellular physiology · 2022
    Article
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  20. Article

2 more citing papers are in PubMed but not listed here.

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

5 authors at 2 institutions in 1 country.

L Contreras-RuizDepartment of Ophthalmology, Boston University School of Medicine, Boston, MA 02118, USA.
A Ghosh-MitraDepartment of Ophthalmology, Harvard Medical School, Schepens Eye Research Institute and Massachusetts Eye and Ear, Boston, MA 02114, USA.
M A ShatosDepartment of Ophthalmology, Harvard Medical School, Schepens Eye Research Institute and Massachusetts Eye and Ear, Boston, MA 02114, USA.
D A DarttDepartment of Ophthalmology, Harvard Medical School, Schepens Eye Research Institute and Massachusetts Eye and Ear, Boston, MA 02114, USA.
S MasliDepartment of Ophthalmology, Boston University School of Medicine, Boston, MA 02118, USA.
Massachusetts Eye and Ear Infirmary · USBoston University · US

Funding

Conjunctival Goblet Cell Mucin Secretion in Inflammation and Its ResolutionR01EY019470 · NEI · SCHEPENS EYE RESEARCH INSTITUTE · PI DARTT, DARLENE A · 2009 to 2023
$7.4M
Molecular Mechanisms Underlying Immune Regulation of Ocular InflammationR01EY015472 · NEI · SCHEPENS EYE RESEARCH INSTITUTE · PI MASLI, SHARMILA · 2004 to 2013
$4.3M
NEI NIH HHS EY015472NEI NIH HHS R01 EY015472NEI NIH HHS R01 EY019470
6 · The paper itself

Abstract

Ocular surface inflammation associated with Sjögren's syndrome is characterized by a loss of secretory function and alteration in numbers of mucin secreting goblet cells. Such changes are a prominent feature of ocular surface inflammatory diseases and are attributed to inflammation; however, the exact effect of the inflammatory cytokines on conjunctival goblet cell function remains largely unknown. In this study, we developed a primary culture of mouse goblet cells from conjunctival tissue and evaluated the effects on their function by inflammatory cytokines detected in the conjunctiva of mouse model of Sjögren's syndrome (Thrombospondin-1 deficient mice). We found that apoptosis of goblet cells was primarily induced by TNF-α and IFN-γ. These two cytokines also inhibited mucin secretion by goblet cells in response to cholinergic stimulation, whereas IL-6 enhanced such secretion. No changes in secretory response were detected in the presence of IL-13 or IL-17. Goblet cells proliferated to varying degrees in response to all the tested cytokines with the greatest response to IL-13 followed by IL-6. Our results therefore reveal that inflammatory cytokines expressed in the conjunctiva during an ocular surface disease directly disrupt conjunctival goblet cell functions, compromising the protective function of tears, thereby contributing to ocular surface damage.

Indexed as

AnimalsApoptosisCarbacholCell ProliferationCells, CulturedConjunctivaCytokinesGoblet CellsMiceMice, Inbred C57BLMucin 5ACReceptors, CytokineTh2 CellsThrombospondin 1CarbacholCytokinesMuc5ac protein, mouseMucin 5ACReceptors, CytokineThrombospondin 1

Identifiers

PMID24453426
PMCPMC3877636
OpenAlexW2112421427

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.