Evidence map›Paper›PMID 26517273›Full record

ArticlePloS one2015

Neutrophils as a Source of Chitinases and Chitinase-Like Proteins in Type 2 Diabetes.

Ewa Żurawska-Płaksej, Agnieszka Ługowska, Katarzyna Hetmańczyk, Maria Knapik-Kordecka, Agnieszka Piwowar

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

19 citing papers in PubMed, 36 citations in OpenAlex.

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  10. Defense Mechanisms of CottonInternational journal of molecular sciences · 2022
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  13. Chitotriosidase: a marker and modulator of lung disease.European respiratory review : an official journal of the European Respiratory Society · 2020
    Review
  14. Article
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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

5 authors at 2 institutions in 1 country.

Ewa Żurawska-PłaksejDepartment of Pharmaceutical Biochemistry, Wroclaw Medical University, Wroclaw, Poland.
Agnieszka ŁugowskaDepartment of Genetics, Institute of Psychiatry and Neurology in Warsaw, Warsaw, Poland.
Katarzyna HetmańczykDepartment of Genetics, Institute of Psychiatry and Neurology in Warsaw, Warsaw, Poland.
Maria Knapik-KordeckaDepartment of Angiology, Hypertension and Diabetology, Wroclaw Medical University, Wroclaw, Poland.
Agnieszka PiwowarDepartment of Toxicology, Wroclaw Medical University, Wroclaw, Poland.
Wroclaw Medical University · PLInstitute of Psychiatry and Neurology · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeThe pathophysiological role of human chitinases and chitinase-like proteins (CLPs) is not fully understood. We aimed to determine the levels of neutrophil-derived chitotriosidase (CHIT1), acidic mammalian chitinase (AMCase) and chitinase 3-like protein 1 (YKL-40) in patients with type 2 diabetes (T2D) and verify their association with metabolic and clinical conditions of these patients.

methodsNeutrophils were obtained from the whole blood by gradient density centrifugation from 94 T2D patients and 40 control subjects. The activities of CHIT1 and AMCase as well as leukocyte elastase (LE) were measured fluorometrically and concentration of YKL-40 immunoenzymatically. Also, routine laboratory parameters in serum/plasma were determined by standard methods.

resultsThe levels of all three examined proteins were about 2-times higher in diabetic patients in comparison to control subjects. They were significantly correlated with the activity of LE and increased progressively across tertiles of LE activity. Moreover, the activities of CHIT1 and AMCase were significantly correlated with each other. Metabolic compensation of diabetes did not influence the levels of these proteins. In the subgroup of patients with inflammatory evidence only YKL-40 concentration was significantly higher compared to those without inflammation. The highest levels of all three proteins were observed in patients with macroangiopathies. Insulin therapy was associated with lower levels of examined proteins.

conclusionsWe revealed that neutrophils may be an important source of the increased levels of chitinases and CLPs in T2D, and these proteins may participate in inflammatory mechanisms in the course of the disease and consequent development of diabetic angiopathies.

Indexed as

AdipokinesCase-Control StudiesChitinase-3-Like Protein 1ChitinasesDiabetes Mellitus, Type 2Diabetic AngiopathiesGene Expression RegulationHexosaminidasesHumansInsulinLectinsNeutrophilsAdipokinesCHI3L1 protein, humanCHIA protein, humanChitinase-3-Like Protein 1ChitinaseschitotriosidaseHexosaminidasesInsulinLectins

Identifiers

PMID26517273
PMCPMC4627817
OpenAlexW1946961399

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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.