Evidence map›Paper›PMID 20089077›Full record

ArticleClinical and experimental immunology2010

The increased mucosal mRNA expressions of complement C3 and interleukin-17 in inflammatory bowel disease.

T Sugihara, A Kobori, H Imaeda, T Tsujikawa, K Amagase, K Takeuchi, Y Fujiyama, A Andoh

Open access · greenAbstract read
In one paragraph

Article in Clinical and experimental immunology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed, 1 pooled it
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

59 citing papers in PubMed, 1 synthesis or guideline pooled it, 128 citations in OpenAlex.

  1. Pooled it
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  14. Complement C3-Deficiency-Induced Constipation in FVB/N-C3International journal of molecular sciences · 2023
    Article
  15. Article
  16. IgA nephropathy associated with Crohn's disease.World journal of methodology · 2023
    Review
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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 2 institutions in 1 country.

T SugiharaDepartment of Medicine, Shiga University of Medical Science, Otsu, Japan.
A Kobori
H Imaeda
T Tsujikawa
K Amagase
K Takeuchi
Y Fujiyama
A Andoh
Shiga University of Medical Science · JPKyoto Pharmaceutical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent studies have demonstrated that the complement system participates in the regulation of T cell functions. To address the local biosynthesis of complement components in inflammatory bowel disease (IBD) mucosa, we investigated C3 and interleukin (IL)-17 mRNA expression in mucosal samples obtained from patients with IBD. The molecular mechanisms underlying C3 induction were investigated in human colonic subepithelial myofibroblasts (SEMFs). IL-17 and C3 mRNA expressions in the IBD mucosa were evaluated by real-time polymerase chain reaction. The C3 levels in the supernatant were determined by enzyme-linked immunosorbent assay. IL-17 and C3 mRNA expressions were elevated significantly in the active lesions from ulcerative colitis (UC) and Crohn's disease (CD) patients. There was a significant positive correlation between IL-17 and C3 mRNA expression in the IBD mucosa. IL-17 stimulated a dose- and time-dependent increase in C3 mRNA expression and C3 secretion in colonic SEMFs. The C3 molecules secreted by colonic SEMFs were a 115-kDa alpha-chain linked to a 70-kDa beta-chain by disulphide bonds, which was identical to serum C3. The IL-17-induced C3 mRNA expression was blocked by p42/44 mitogen-activated protein kinase (MAPK) inhibitors (PD98059 and U0216) and a p38 MAPK inhibitor (SB203580). Furthermore, IL-17-induced C3 mRNA expression was inhibited by an adenovirus containing a stable mutant form of I kappaB alpha. C3 and IL-17 mRNA expressions are enhanced, with a strong correlation, in the inflamed mucosa of IBD patients. Part of these clinical findings was considered to be mediated by the colonic SEMF response to IL-17.

Indexed as

AdenoviridaeColitis, UlcerativeColonComplement C3Crohn DiseaseDose-Response Relationship, DrugEnzyme InhibitorsFemaleFlavonoidsGene Expression RegulationHumansI-kappa B ProteinsImidazolesInterleukin-17Intestinal MucosaMale2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-oneComplement C3Enzyme InhibitorsFlavonoidsI-kappa B ProteinsImidazolesInterleukin-17Mitogen-Activated Protein Kinase 1NF-KappaB Inhibitor alphaNFKBIA protein, humanp38 Mitogen-Activated Protein KinasesPyridinesRNA, MessengerSB 203580

Identifiers

PMID20089077
PMCPMC2883109
OpenAlexW1589464081

What OpenQuestion holds

Textmetadata
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.