Evidence map›Paper›PMID 24385947›Full record

ArticleImmune network2013

BIRB 796 has Distinctive Anti-inflammatory Effects on Different Cell Types.

Soyoon Ryoo, Jida Choi, Jaemyung Kim, Suyoung Bae, Jaewoo Hong, Seunghyun Jo, Soohyun Kim, Youngmin Lee

Open access · hybridAbstract read
In one paragraph

Article in Immune network, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.0field-weighted citation impact, top 24% 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

7 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Review
  3. Microcystin-LR (MC-LR) Triggers Inflammatory Responses in Macrophages.International journal of molecular sciences · 2021
    Article
  4. Review
  5. Article
  6. Article
  7. 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

8 authors at 4 institutions in 1 country.

Soyoon RyooLaboratory of Cytokine Immunology, Department of Biomedical Sciences and Technology, Konkuk University, Seoul 143-701, Korea. ; Division of Veterinary Bacterial Disease Division, Animal and Plant Quarantine Agency, Gyeonggi-do 480-757, Korea.
Jida ChoiLaboratory of Cytokine Immunology, Department of Biomedical Sciences and Technology, Konkuk University, Seoul 143-701, Korea. ; Division of Veterinary Epidemiology, Animal and Plant Quarantine Agency, Gyeonggi-do 480-757, Korea.
Jaemyung KimDivision of Veterinary Bacterial Disease Division, Animal and Plant Quarantine Agency, Gyeonggi-do 480-757, Korea.
Suyoung BaeLaboratory of Cytokine Immunology, Department of Biomedical Sciences and Technology, Konkuk University, Seoul 143-701, Korea. ; Department of Bioequivalence Division for Drug Evaluation, Ministry of Food and Drug Safety, Chungcheongbuk-do 363-700, Korea.
Jaewoo HongLaboratory of Cytokine Immunology, Department of Biomedical Sciences and Technology, Konkuk University, Seoul 143-701, Korea.
Seunghyun JoLaboratory of Cytokine Immunology, Department of Biomedical Sciences and Technology, Konkuk University, Seoul 143-701, Korea.
Soohyun KimLaboratory of Cytokine Immunology, Department of Biomedical Sciences and Technology, Konkuk University, Seoul 143-701, Korea.
Youngmin LeeDepartment of Medicine, Pusan Paik Hospital, Collage of Medicine, Inje University, Busan 633-165, Korea.
Konkuk University · KRAnimal and Plant Quarantine Agency · KRInje University Busan Paik Hospital · KRMinistry of Food and Drug Safety · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The pro-inflammatory cytokines tumor necrosis factor-α (TNFα) and interleukin (IL)-1β are crucial mediators involved in chronic inflammatory diseases. Inflammatory signal pathways regulate inflammatory cytokine expression-mediated by p38 mitogen activated protein kinase (p38MAPK). Therefore, considerable attention has been given to p38MAPK as a target molecule for the development of a novel anti-inflammatory therapeutics. BIRB 796, one of p38MAPK inhibitor, is a candidate of therapeutic drug for chronic inflammatory diseases. In this study, we investigated the effect of BIRB 796 on inflammatory cytokine productions by lipopolysaccharide (LPS) in different immune cell types. BIRB 796 reduced LPS-mediated IL-8 production in THP-1 cells but not in Raw 264.7 cells. Further analysis of signal molecules by western blot revealed that BIRB 796 sufficiently suppressed LPS-mediated phosphorylation of p38MAPK in both cell types whereas it failed to block inhibitor of kappa B (I-κB) degradation in Raw 264.7 cells. Taken together, these results suggest that the anti-inflammatory function of BIRB 796 depends on cell types.

Indexed as

BIRB 796Inflammatory cytokineInflammatory signal pathwaysLPSp38MAPK

Identifiers

PMID24385947
PMCPMC3875787
OpenAlexW1983046473

What OpenQuestion holds

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LicenceCC BY-NC
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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.