Evidence map›Paper›PMID 34054686›Full record

ArticleFrontiers in neurology2021

Monocyte-Derived Macrophages Contribute to Chitinase Dysregulation in Amyotrophic Lateral Sclerosis: A Pilot Study.

Nayana Gaur, Elena Huss, Tino Prell, Robert Steinbach, Joel Guerra, Akash Srivastava, Otto W Witte, Julian Grosskreutz

Open access · goldAbstract read
In one paragraph

Article in Frontiers in neurology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.8field-weighted citation impact, top 26% 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

10 citing papers in PubMed, 8 citations in OpenAlex.

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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

8 authors at 1 institution in 1 country.

Nayana GaurHans Berger Department of Neurology, Jena University Hospital, Jena, Germany.
Elena HussHans Berger Department of Neurology, Jena University Hospital, Jena, Germany.
Tino PrellHans Berger Department of Neurology, Jena University Hospital, Jena, Germany.
Robert SteinbachHans Berger Department of Neurology, Jena University Hospital, Jena, Germany.
Joel GuerraDepartment of Anaesthesiology and Intensive Care Medicine, Jena University Hospital, Jena, Germany.
Akash SrivastavaHans Berger Department of Neurology, Jena University Hospital, Jena, Germany.
Otto W WitteHans Berger Department of Neurology, Jena University Hospital, Jena, Germany.
Julian GrosskreutzHans Berger Department of Neurology, Jena University Hospital, Jena, Germany.
Jena University Hospital · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neuroinflammation significantly contributes to Amyotrophic Lateral Sclerosis (ALS) pathology. In lieu of this, reports of elevated chitinase levels in ALS are interesting, as they are established surrogate markers of a chronic inflammatory response. While post-mortem studies have indicated glial expression, the cellular sources for these moieties remain to be fully understood. Therefore, the objective of this pilot study was to examine whether the peripheral immune system also contributes to chitinase dysregulation in ALS. The temporal expression of CHIT1, CHI3L1, and CHI3L2 in non-polarized monocyte-derived macrophages (MoMas) from ALS patients and healthy controls (HCs) was examined. We demonstrate that while CHIT1 and CHI3L1 display similar temporal expression dynamics in both groups, profound between-group differences were noted for these targets at later time-points i.e., when cells were fully differentiated. CHIT1 and CHI3L1 expression were significantly higher in MoMas from ALS patients at both the transcriptomic and protein level, with CHI3L1 levels also being influenced by age. Conversely, CHI3L2 expression was not influenced by disease state, culture duration, or age. Here, we demonstrate for the first time, that in ALS, circulating immune cells have an intrinsically augmented potential for chitinase production that may propagate chronic neuroinflammation, and how the ageing immune system itself contributes to neurodegeneration.

Indexed as

ageingchitinasesmacrophagesneurodegenerationneuroinflammation

Identifiers

PMID34054686
PMCPMC8160083
OpenAlexW3163526177

What OpenQuestion holds

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LicenceCC BY
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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.