Evidence map›Paper›PMID 28704475›Full record

ArticlePloS one2017

Protective effect of Galectin-9 in murine model of lung emphysema: Involvement of neutrophil migration and MMP-9 production.

Yuko Horio, Hidenori Ichiyasu, Keisuke Kojima, Naoki Saita, Yohei Migiyama, Toyohisa Iriki, Kazuhiko Fujii, Toshiro Niki, Mitsuomi Hirashima, Hirotsugu Kohrogi

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing 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

11 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
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  3. EndothelialResearch square · 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

10 authors at 2 institutions in 1 country.

Yuko HorioDepartment of Respiratory Medicine, Faculty of Life Sciences, Kumamoto University, Kumamoto, Japan.
Hidenori IchiyasuDepartment of Respiratory Medicine, Faculty of Life Sciences, Kumamoto University, Kumamoto, Japan.
Keisuke KojimaDepartment of Respiratory Medicine, Faculty of Life Sciences, Kumamoto University, Kumamoto, Japan.
Naoki SaitaDepartment of Respiratory Medicine, Faculty of Life Sciences, Kumamoto University, Kumamoto, Japan.
Yohei MigiyamaDepartment of Respiratory Medicine, Faculty of Life Sciences, Kumamoto University, Kumamoto, Japan.
Toyohisa IrikiDepartment of Respiratory Medicine, Faculty of Life Sciences, Kumamoto University, Kumamoto, Japan.
Kazuhiko FujiiDepartment of Respiratory Medicine, Faculty of Life Sciences, Kumamoto University, Kumamoto, Japan.
Toshiro NikiDepartment of Immunology and Immunopathology, Kagawa University, Kagawa, Japan.
Mitsuomi HirashimaDepartment of Immunology and Immunopathology, Kagawa University, Kagawa, Japan.
Hirotsugu KohrogiDepartment of Respiratory Medicine, Faculty of Life Sciences, Kumamoto University, Kumamoto, Japan.
Kumamoto University · JPKagawa University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeChronic obstructive pulmonary disease (COPD) is characterized by irreversible airflow obstruction and pulmonary emphysema. Persistent inflammation and remodeling of the lungs and airways result in reduced lung function and a lower quality of life. Galectin (Gal)-9 plays a crucial role as an immune modulator in various diseases. However, its role in the pathogenesis of pulmonary emphysema is unknown. This study investigates whether Gal-9 is involved in pulmonary inflammation and changes in emphysema in a porcine pancreatic elastase (PPE)-induced emphysema model. MATERIALS AND

methodsGal-9 was administered to mice subcutaneously once daily from 1 day before PPE instillation to day 5. During the development of emphysema, lung tissue and bronchoalveolar lavage fluid (BALF) were collected. Histological and cytological findings, concentrations of chemokines and matrix metalloproteinases (MMPs) in the BALF, and the influence of Gal-9 treatment on neutrophils were analyzed.

resultsGal-9 suppressed the pathological changes of PPE-induced emphysema. The mean linear intercept (Lm) of Gal-9-treated emphysema mice was significantly lower than that of PBS-treated emphysema mice (66.1 ± 3.3 μm vs. 118.8 ± 14.8 μm, respectively; p < 0.01). Gal-9 decreased the number of neutrophils and levels of MMP-9, MMP-2 and tissue inhibitor of metalloproteinases (TIMP)-1 in the BALF. The number of neutrophils in the BALF correlated significantly with MMPs levels. Interestingly, Gal-9 pretreatment in vitro inhibited the chemotactic activity of neutrophils and MMP-9 production from neutrophils. Furthermore, in Gal-9-deficient mice, PPE-induced emphysema progressed significantly compared with that in wild-type (WT) mice (108.7 ± 6.58 μm vs. 77.19 ± 6.97 μm, respectively; p < 0.01).

conclusionsThese results suggest that Gal-9 protects PPE-induced inflammation and emphysema by inhibiting the infiltration of neutrophils and decreasing MMPs levels. Exogenous Gal-9 could be a potential therapeutic agent for COPD.

Indexed as

AnimalsChemotaxisFemaleGalectinsMatrix Metalloproteinase 2Matrix Metalloproteinase 9MiceMice, Inbred C57BLNeutrophilsPulmonary Emphysemagalectin 9, mouseGalectinsMatrix Metalloproteinase 2Matrix Metalloproteinase 9Mmp2 protein, mouseMmp9 protein, mouse

Identifiers

PMID28704475
PMCPMC5507541
OpenAlexW2735051971

What OpenQuestion holds

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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.