Evidence map›Paper›PMID 28872665›Full record

ArticleClinical and experimental immunology2018

Expression of human cathelicidin peptide LL-37 in inflammatory bowel disease.

S Kusaka, A Nishida, K Takahashi, S Bamba, H Yasui, M Kawahara, O Inatomi, M Sugimoto, A Andoh

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Clinical and experimental immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.9field-weighted citation impact, top 10% 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

23 citing papers in PubMed, 41 citations in OpenAlex.

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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

9 authors at 2 institutions in 1 country.

S KusakaDepartment of Medicine, Shiga University of Medical Science, Otsu, Japan.
A NishidaDepartment of Medicine, Shiga University of Medical Science, Otsu, Japan.ORCID 0000-0002-1288-3272
K TakahashiDepartment of Medicine, Shiga University of Medical Science, Otsu, Japan.
S BambaDepartment of Medicine, Shiga University of Medical Science, Otsu, Japan.
H YasuiDepartment of Analytical and Bioinorganic Chemistry, Kyoto Pharmaceutical University, Kyoto, Japan.
M KawaharaDepartment of Medicine, Shiga University of Medical Science, Otsu, Japan.
O InatomiDepartment of Medicine, Shiga University of Medical Science, Otsu, Japan.
M SugimotoDepartment of Medicine, Shiga University of Medical Science, Otsu, Japan.
A AndohDepartment of Medicine, Shiga University of Medical Science, Otsu, Japan.
Shiga University of Medical Science · JPKyoto Pharmaceutical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cathelicidin peptide LL-37 plays an important role in the early host response against invading pathogens via its broad-spectrum anti-microbial activity. In this study, we investigated LL-37 expression in the inflamed mucosa of inflammatory bowel disease (IBD) patients. Furthermore, the regulatory mechanism of LL-37 induction was investigated in human colonic subepithelial myofibroblasts (SEMFs). LL-37 mRNA expression and protein secretion were analysed using real-time polymerase chain reaction and enzyme-linked immunosorbent assay, respectively. Intracellular signalling pathways were analysed using immunoblotting and specific small interference RNA (siRNA). The expression of LL-37 mRNA was increased significantly in the inflamed mucosa of ulcerative colitis and Crohn's disease. The Toll-like receptor (TLR)-3 ligand, polyinosinic-polycytidylic acid (poly(I:C), induced LL-37 mRNA expression and stimulated LL-37 secretion in colonic SEMFs. The transfection of siRNAs specific for intracellular signalling proteins [Toll/IL-1R domain-containing adaptor-inducing interferon (IFN) (TRIF), tumour necrosis factor receptor-associated factor (TRAF)6, transforming growth factor β-activated kinase (TAK)1] suppressed the poly(I:C)-induced LL-37 mRNA expression significantly. Poly(I:C)-induced phosphorylation of mitogen-activated protein kinases (MAPKs) and activated nuclear factor kappa B (NF-κB) and activating factor protein (AP)-1. siRNAs specific for NF-κB and c-Jun inhibited poly(I:C)-induced LL-37 mRNA expression. LL-37 suppressed lipopolysaccharide (LPS)-induced interleukin (IL)-6 and IL-8 expression significantly in colonic SEMFs. The expression of LL-37 was up-regulated in the inflamed mucosa of IBD patients. LL-37 was induced by TLR-3 stimulation and exhibited an anti-microbial effect via interaction with lipopolysaccharide (LPS).

Indexed as

Gene Expression RegulationAdaptor Proteins, Vesicular TransportAntimicrobial Cationic PeptidesBiomarkersCathelicidinsColonCytokinesHumansImmunohistochemistryInflammation MediatorsInflammatory Bowel DiseasesIntestinal MucosaIntracellular Signaling Peptides and ProteinsMAP Kinase Kinase Kinase 7MAP Kinase Kinase KinasesMyofibroblastsAdaptor Proteins, Vesicular TransportAntimicrobial Cationic PeptidesBiomarkersCathelicidinsCytokinesInflammation MediatorsIntracellular Signaling Peptides and ProteinsMAP Kinase Kinase Kinase 7MAP Kinase Kinase KinasesPoly I-CTICAM1 protein, humanTifab protein, humanTNF Receptor-Associated Factor 6anti-microbial peptidesLL-37myofibroblasts

Identifiers

PMID28872665
PMCPMC5721246
OpenAlexW2752328766

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.