Evidence map›Paper›PMID 32218599›Full record

ArticlePloS one2020

Exacerbation of symptomatic arthritis by cigarette smoke in experimental arthritis.

Jaewoo Kang, Sang Hoon Jeong, Kijun Lee, Narae Park, Hyerin Jung, Kyuhong Lee, Ji Hyeon Ju

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

16 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
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  7. Autoimmunity: A New Focus on Nasal Polyps.International journal of molecular sciences · 2023
    Review
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  11. HLA-G and the MHC Cusp Theory.Frontiers in immunology · 2022
    Review
  12. Article
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  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

7 authors at 3 institutions in 1 country.

Jaewoo KangCiSTEM laboratory, Catholic Induced Pluripotent Stem Cell (iPSC) Research Center, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea.
Sang Hoon JeongCiSTEM laboratory, Catholic Induced Pluripotent Stem Cell (iPSC) Research Center, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea.
Kijun LeeCiSTEM laboratory, Catholic Induced Pluripotent Stem Cell (iPSC) Research Center, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea.
Narae ParkCiSTEM laboratory, Catholic Induced Pluripotent Stem Cell (iPSC) Research Center, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea.
Hyerin JungCiSTEM laboratory, Catholic Induced Pluripotent Stem Cell (iPSC) Research Center, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea.
Kyuhong LeeJeonbuk Department of Inhalation Research, Korea Institute of Toxicology, Jeongeup, Jeollabuk-do, Republic of Korea.
Ji Hyeon JuCiSTEM laboratory, Catholic Induced Pluripotent Stem Cell (iPSC) Research Center, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea.ORCID 0000-0002-1381-5466
The Catholic University of Korea Seoul St. Mary's Hospital · KRKorea Institute of Toxicology · KRCatholic University of Korea · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionEpidemiologically, cigarette smoking is a well-known risk factor for the pathogenesis of rheumatoid arthritis (RA). However, there has been few plausible explanations why cigarette smoking aggravated RA. We investigated the causal effect of smoking in experimental model of arthritis development.

methodsDuring induction of experimental arthritis with collagen challenge, mice were exposed to a smoking environment with 3R4F cigarettes. Generated smoke was delivered to mice through a nose-only exposure chamber (ISO standard 3308). Human cartilage pellet was challenged by cigarette smoke extract to identify citrullinating potential in vitro.

resultsCigarette smoke exacerbated arthritis in a collagen-induced arthritis (CIA) model. Exposure to smoke accelerated the onset of arthritis by 2 weeks compared to the conventional model without smoke. Citrullination of lung tissue as well as tarsal joints were revealed in smoke-aggravated CIA mice. Interestingly, tracheal cartilage was a core organ regarding intensity and area size of citrullination. The trachea might be an interesting organ in viewpoint of sharing cartilage with joint and direct smoke exposure. Anti-CCP antibodies were barely detected in the serum of CIA mice, they were significantly elevated in cigarette smoke group. Citrullinated antigens were increased in the serum of smoke-exposed mice. Lastly, a cigarette smoke extract enhanced human cartilage citrullination in vitro.

conclusionsMissing link of arthritic mechanism between smoke and RA could be partially explained by tracheal citrullination. To control tracheal cartilage citrullination may be beneficial for preventing arthritis development or aggravation if cigarette smoke is becoming a risk factor to pre-arthritic individual.

Indexed as

AnimalsArthritis, ExperimentalCigarette SmokingCitrullinationFemaleMiceRespiratory System

Identifiers

PMID32218599
PMCPMC7100974
OpenAlexW3013899416

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.