Evidence map›Paper›PMID 36341422›Full record

ArticleFrontiers in immunology2022

Role of periostin in inflammatory bowel disease development and synergistic effects mediated by the CCL5-CCR5 axis.

Saida Mukanova, Anton Borissenko, Alexey Kim, Aigerim Bolatbek, Ainur Abdrakhmanova, Luca Vangelista, Eva Sonnenberg-Riethmacher, Dieter Riethmacher

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.1field-weighted citation impact, top 11% 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

15 citing papers in PubMed, 13 citations in OpenAlex.

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  7. CD74Journal of translational medicine · 2025
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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 2 countries.

Saida MukanovaDepartment of Biomedical Sciences, School of Medicine, Nazarbayev University, Astana, Kazakhstan.
Anton BorissenkoDepartment of Biomedical Sciences, School of Medicine, Nazarbayev University, Astana, Kazakhstan.
Alexey KimSchool of Medicine, Nazarbayev University, Astana, Kazakhstan.
Aigerim BolatbekDepartment of Biomedical Sciences, School of Medicine, Nazarbayev University, Astana, Kazakhstan.
Ainur AbdrakhmanovaSchool of Medicine, Nazarbayev University, Astana, Kazakhstan.
Luca VangelistaDepartment of Biomedical Sciences, School of Medicine, Nazarbayev University, Astana, Kazakhstan.
Eva Sonnenberg-RiethmacherDepartment of Biomedical Sciences, School of Medicine, Nazarbayev University, Astana, Kazakhstan.
Dieter RiethmacherDepartment of Biomedical Sciences, School of Medicine, Nazarbayev University, Astana, Kazakhstan.
Nazarbayev University · KZUniversity of Southampton · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inflammatory bowel disease (IBD), comprising mainly Crohn's disease (CD) and ulcerative colitis (UC), is a chronic inflammatory disease of the gastrointestinal tract. In recent years, a wealth of data has been accumulated demonstrating the complex interplay of many different factors in the pathogenesis of IBD. Among these are factors impacting the epithelial barrier function, including vessel and extracellular matrix (ECM) formation, the gut microbiome (e.g., bacterial antigens), and, most importantly, the production of cytokines (pro- and anti-inflammatory) directly shaping the immune response. Patients failing to resolve the acute intestinal inflammation develop chronic inflammation. It has been shown that the expression of the matricellular protein periostin is enhanced during IBD and is one of the drivers of this disease. The C-C chemokine receptor 5 (CCR5) is engaged by the chemotactic mediators CCL3/MIP-1α, CCL4/MIP-1β, and CCL5/RANTES. CCR5 blockade has been reported to ameliorate inflammation in a murine IBD model. Thus, both periostin and CCR5 are involved in the development of IBD. In this study, we investigated the potential crosstalk between the two signaling systems and tested a highly potent CCL5 derivative acting as a CCR5 antagonist in a murine model of IBD. We observed that the absence of periostin influences the CCR5-expressing cell population of the gut. Our data further support the notion that targeted modulation of the periostin and CCR5 signaling systems bears therapeutic potential for IBD.

Indexed as

Inflammatory Bowel DiseasesReceptors, ChemokineAnimalsChemokine CCL3Chemokine CCL4Chemokine CCL5HumansInflammationMiceReceptors, CCR5CCL5 protein, humanCCR5 protein, humanChemokine CCL3Chemokine CCL4Chemokine CCL5Receptors, CCR5Receptors, ChemokineCCL5-CCR5-signaling systemchemically induced colitisIBD – inflammatory bowel diseaseinflammationperiostin (POSTN)treatment option

Identifiers

PMID36341422
PMCPMC9632729
OpenAlexW4306884713

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.