Evidence map›Paper›PMID 34067842›Full record

ArticlePharmaceuticals (Basel, Switzerland)2021

Treatment with an Anti-CX3CL1 Antibody Suppresses M1 Macrophage Infiltration in Interstitial Lung Disease in SKG Mice.

Satoshi Mizutani, Junko Nishio, Kanoh Kondo, Kaori Motomura, Zento Yamada, Shotaro Masuoka, Soichi Yamada, Sei Muraoka, Naoto Ishii, Yoshikazu Kuboi and 4 more

Open access · goldAbstract read
In one paragraph

Article in Pharmaceuticals (Basel, Switzerland), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

13 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
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

14 authors at 3 institutions in 1 country.

Satoshi MizutaniDepartment of Internal Medicine, Division of Rheumatology, Toho University School of Medicine, Ota-ku, Tokyo 143-8541, Japan.ORCID 0000-0002-4321-5357
Junko NishioDepartment of Internal Medicine, Division of Rheumatology, Toho University School of Medicine, Ota-ku, Tokyo 143-8541, Japan.
Kanoh KondoDepartment of Internal Medicine, Division of Rheumatology, Toho University School of Medicine, Ota-ku, Tokyo 143-8541, Japan.
Kaori MotomuraDepartment of Internal Medicine, Division of Rheumatology, Toho University School of Medicine, Ota-ku, Tokyo 143-8541, Japan.
Zento YamadaDepartment of Internal Medicine, Division of Rheumatology, Toho University School of Medicine, Ota-ku, Tokyo 143-8541, Japan.
Shotaro MasuokaDepartment of Internal Medicine, Division of Rheumatology, Toho University School of Medicine, Ota-ku, Tokyo 143-8541, Japan.
Soichi YamadaDepartment of Internal Medicine, Division of Rheumatology, Toho University School of Medicine, Ota-ku, Tokyo 143-8541, Japan.
Sei MuraokaDepartment of Internal Medicine, Division of Rheumatology, Toho University School of Medicine, Ota-ku, Tokyo 143-8541, Japan.ORCID 0000-0002-9853-8057
Naoto IshiiKAN Research Institute, Inc., Chuo-ku, Kobe-shi, Hyogo 650-0047, Japan.
Yoshikazu KuboiKAN Research Institute, Inc., Chuo-ku, Kobe-shi, Hyogo 650-0047, Japan.
Sho SendoDepartment of Internal Medicine, Division of Rheumatology and Clinical Immunology, Kobe University Graduate School of Medicine, Chuo-ku, Kobe-shi, Hyogo 650-0017, Japan.
Tetuo MikamiDepartment of Pathology, Toho University School of Medicine, Ota-ku, Tokyo 143-8540, Japan.
Toshio ImaiKAN Research Institute, Inc., Chuo-ku, Kobe-shi, Hyogo 650-0047, Japan.
Toshihiro NankiDepartment of Internal Medicine, Division of Rheumatology, Toho University School of Medicine, Ota-ku, Tokyo 143-8541, Japan.ORCID 0000-0002-3482-074X
Toho University · JPKAN Research Institute · JPKobe University · JP

Funding

Early-Career Scientists 19K17897Grants-in-Aid for Scientific Research (C) 18K07166Research Promotion Grant from the Toho University Graduate School of Medicine No. 17-01, 20-01the Private University Research Branding Project from the Ministry of Education, Culture, Sports, Science, and Technology no numberthe Program for the Strategic Research Foundation for Private Universities S1411015
6 · The paper itself

Abstract

CX3C Motif Chemokine Ligand 1 (CX3CL1; fractalkine) has been implicated in the pathogenesis of rheumatoid arthritis (RA) and its inhibition was found to attenuate arthritis in mice as well as in a clinical trial. Therefore, we investigated the effects of an anti-CX3CL1 monoclonal antibody (mAb) on immune-mediated interstitial lung disease (ILD) in SKG mice, which exhibit similar pathological and clinical features to human RA-ILD. CX3CL1 and CX3C chemokine receptor 1 (CX3CR1), the receptor for CX3CL1, were both expressed in the fibroblastic foci of lung tissue and the number of bronchoalveolar fluid (BALF) cells was elevated in ILD in SKG mice. No significant changes were observed in lung fibrosis or the number of BALF cells by the treatment with anti-CX3CL1 mAb. However, significantly greater reductions were observed in the number of M1 macrophages than in M2 macrophages in the BALF of treated mice. Furthermore, CX3CR1 expression levels were significantly higher in M1 macrophages than in M2 macrophages. These results suggest the stronger inhibitory effects of the anti-CX3CL1 mAb treatment against the alveolar infiltration of M1 macrophages than M2 macrophages in ILD in SKG mice. Thus, the CX3CL1-CX3CR1 axis may be involved in the infiltration of inflammatory M1 macrophages in RA-ILD.

Indexed as

CX3CL1/fractalkineCX3CR1interstitial lung diseasesM1 macrophageM2 macrophagerheumatoid arthritisSKG mice

Identifiers

PMID34067842
PMCPMC8156344
OpenAlexW3160390448

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.