Evidence map›Paper›PMID 35620349›Full record

ArticleInternational journal of chronic obstructive pulmonary disease2022

Glucose Homeostasis in Relation to Neutrophil Mobilization in Smokers with COPD.

Nikolaos Pournaras, Anders Andersson, Melissa A Kovach, Médea Padra, Karlhans F Che, Bettina Brundin, Shigemi Yoshihara, Steven Bozinovski, Sara K Lindén, Per-Anders Jansson and 3 more

Open access · goldAbstract read
In one paragraph

Article in International journal of chronic obstructive pulmonary disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.2field-weighted citation impact, top 52% 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

1 citing paper in PubMed, 1 citations in OpenAlex.

  1. Review
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

13 authors at 6 institutions in 3 countries.

Nikolaos PournarasDivision for Lung and Airway Research, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.ORCID 0000-0002-9693-3838
Anders AnderssonCOPD Center, Department of Respiratory Medicine and Allergology, Sahlgrenska University Hospital, Gothenburg, Sweden.
Melissa A KovachDivision for Lung and Airway Research, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
Médea PadraInstitute of Biomedicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Karlhans F CheDivision for Lung and Airway Research, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
Bettina BrundinDivision for Lung and Airway Research, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
Shigemi YoshiharaPediatric Allergology and Respiratory Medicine, Department of Pediatrics, Dokkyo Medical University, Mibu, Tochigi, Japan.
Steven BozinovskiSchool of Health and Biomedical Sciences, RMIT University, Bundoora, Victoria, Australia.
Sara K LindénInstitute of Biomedicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Per-Anders JanssonInstitute of Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Magnus C SköldKarolinska Severe COPD Center, Department of Respiratory Medicine and Allergy, Karolinska University Hospital, Stockholm, Sweden.
Ingemar QvarfordtCOPD Center, Department of Respiratory Medicine and Allergology, Sahlgrenska University Hospital, Gothenburg, Sweden.
Anders LindénDivision for Lung and Airway Research, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.ORCID 0000-0003-1258-2928
Karolinska University Hospital · SEUniversity of Gothenburg · SEKarolinska Institutet · SESahlgrenska University Hospital · SEDokkyo Medical University · JPRMIT University · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Purpose: Type 2 diabetes mellitus (T2DM) and metabolic syndrome (MetS) are common comorbidities in chronic obstructive pulmonary disease (COPD), but the underlying pathogenic mechanisms are poorly understood. Given that these morbidities all display increased neutrophil mobilization, the current study aimed to address whether glucose homeostasis relates to signs of neutrophil mobilization in COPD. Methods: The study population included healthy non-smokers (HNS) and long-term smokers without (LTS) and with COPD (LTS+COPD). No subject had T2DM or MetS. Serum cotinine was quantified to evaluate current smoking. Capillary blood glucose was measured after overnight fasting and during an oral glucose tolerance test (OGTT). Neutrophils were quantified in blood and bronchoalveolar lavage samples (BAL). The neutrophil-related cytokines IL-36α, -β and -γ were quantified (ELISA) along with IL-6, IL-8, INF-γ and CXCL10 (U-Plex Results: The LTS+COPD group had lower fasting glucose, greater change in glucose during OGTT and higher neutrophil concentrations in BAL and blood compared with HNS. Fasting glucose correlated in a positive manner with blood neutrophil concentration, forced expiratory volume in 1 second/forced vital capacity ratio (FEV Conclusion: In smokers with COPD, altered glucose homeostasis is associated with local and systemic signs of increased neutrophil mobilization, but not with local proteinases. This suggests that other specific aspects of neutrophil mobilization constitute pathogenic factors that affect glucose homeostasis in COPD.

Indexed as

Diabetes Mellitus, Type 2Pulmonary Disease, Chronic ObstructiveGlucoseHomeostasisHumansLeukocyte ElastaseNeutrophilsSmokersGlucoseLeukocyte ElastaseBALelastasegranulocyteIL-36IP-10

Identifiers

PMID35620349
PMCPMC9129100
OpenAlexW4281728175

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Registered trials

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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.