Evidence map›Paper›PMID 32410713›Full record

ArticleArthritis research & therapy2020

Targeting a cysteine protease from a pathobiont alleviates experimental arthritis.

Hsin-Yi Peng, Shih-Yao Chen, Shih-Hong Siao, Jinghua Tsai Chang, Ting-Yin Xue, Yi-Hsuan Lee, Ming-Shiou Jan, Gregory J Tsay, Moncef Zouali

Open access · goldAbstract read
In one paragraph

Article in Arthritis research & therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

8 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. Review
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  7. Pathogens (Basel, Switzerland) · 2020
    Review
  8. Microorganisms · 2020
    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

9 authors at 5 institutions in 2 countries.

Hsin-Yi PengDivision of Immunology and Rheumatology, China Medical University Hospital, Taichung, Taiwan.
Shih-Yao ChenDepartment of Internal Medicine, National Cheng Kung University Hospital, Tainan, Taiwan.
Shih-Hong SiaoGraduate Institute of Immunology, National Taiwan University, Taipei, Taiwan.
Jinghua Tsai ChangInstitute of Medicine, Chung Shan Medical University, Taichung, Taiwan.
Ting-Yin XueDivision of Immunology and Rheumatology, China Medical University Hospital, Taichung, Taiwan.
Yi-Hsuan LeeDivision of Immunology and Rheumatology, China Medical University Hospital, Taichung, Taiwan.
Ming-Shiou JanInstitute of Biochemistry, Microbiology, Immunology, Chung Shan Medical University, Taichung, Taiwan.
Gregory J TsayDivision of Immunology and Rheumatology, China Medical University Hospital, Taichung, Taiwan. jjtsay@mail.cmu.edu.tw.
Moncef ZoualiInserm UMR 1132, F-75475, Paris, France. moncef.zouali@wanadoo.fr.
China Medical University · TWChung Shan Medical University · TWInserm · FRNational Cheng Kung University Hospital · TWNational Taiwan University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSeveral lines of evidence suggest that the pathobiont Porphyromonas gingivalis is involved in the development and/or progression of auto-inflammatory diseases. This bacterium produces cysteine proteases, such as gingipain RgpA, endowed with the potential to induce significant bone loss in model systems and in patients.

objectiveWe sought to gain further insight into the role of this pathobiont in rheumatoid arthritis (RA) and to identify novel therapeutic targets for auto-inflammatory diseases.

methodsWe profiled the antibody response to RgPA-specific domains in patient sera. We also tested the potential protective effects of RgpA domains in an experimental arthritis model.

resultsPre-immunization of rats with purified recombinant RgpA domains alleviated arthritis in the joints of the rodents and reduced bone erosion. Using a functional genomics approach at both the mRNA and protein levels, we report that the pre-immunizations reduced arthritis severity by impacting a matrix metalloprotease characteristic of articular injury, a chemokine known to be involved in recruiting inflammatory cells, and three inflammatory cytokines. Finally, we identified an amino acid motif in the RgpA catalytic domain of P. gingivalis that shares sequence homology with type II collagen.

conclusionWe conclude that pre-immunization against gingipain domains can reduce the severity of experimentally induced arthritis. We suggest that targeting gingipain domains by pre-immunization, or, possibly, by small-molecule inhibitors, could reduce the potential of P. gingivalis to translocate to remote tissues and instigate and/or exacerbate pathology in RA, but also in other chronic inflammatory diseases.

Indexed as

AnimalsArthritisCatalytic DomainGingipain Cysteine EndopeptidasesHumansPorphyromonas gingivalisRatsRecombinant ProteinsGingipain Cysteine EndopeptidasesRecombinant ProteinsCollagen-induced arthritisGingipainPeriodontitisPorphyromonas gingivalisRheumatoid arthritis

Identifiers

PMID32410713
PMCPMC7222327
OpenAlexW3028065344

What Socratic 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 Socratic graph.