Evidence map›Paper›PMID 35928254›Full record

ArticleClinical and experimental gastroenterology2022

Downregulated Mucosal Autophagy, Alpha Kinase-1 and IL-17 Signaling Pathways in Active and Quiescent Ulcerative Colitis.

Luiza Moraes Holst, Jonas Halfvarson, Marie Carlson, Charlotte Hedin, Robert Kruse, Carl Mårten Lindqvist, Daniel Bergemalm, Sven Almér, Francesca Bresso, Maria Ling Lundström and 11 more

Open access · goldAbstract read
In one paragraph

Article in Clinical and experimental gastroenterology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
1.3field-weighted citation impact, top 18% 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

3 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
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

21 authors at 9 institutions in 3 countries.

Luiza Moraes HolstDepartment of Microbiology and Immunology, Institute of Biomedicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Jonas HalfvarsonDepartment of Gastroenterology, Faculty of Medicine and Health, Örebro University, Örebro, Sweden.
Marie CarlsonDepartment of Medical Sciences, Uppsala University, Uppsala, Sweden.
Charlotte HedinDepartment of Medicine Solna, Karolinska Institute, Stockholm, Sweden.ORCID 0000-0002-4921-8516
Robert KruseDepartment of Clinical Research Laboratory, Faculty of Medicine and Health, Örebro University, Örebro, Sweden.
Carl Mårten LindqvistSchool of Medical Sciences, Faculty of Medicine and Health, Örebro University, Örebro, Sweden.
Daniel BergemalmDepartment of Gastroenterology, Faculty of Medicine and Health, Örebro University, Örebro, Sweden.
Sven AlmérDepartment of Medicine Solna, Karolinska Institute, Stockholm, Sweden.ORCID 0000-0001-9334-1821
Francesca BressoKarolinska University Hospital, Gastroenterology Unit, Department of Gastroenterology, Dermatovenereology and Rheumatology, Stockholm, Sweden.
Maria Ling LundströmDepartment of Medical Sciences, Uppsala University, Uppsala, Sweden.
Dirk RepsilberSchool of Medical Sciences, Faculty of Medicine and Health, Örebro University, Örebro, Sweden.
Mauro D'AmatoClinical Epidemiology Division, Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden.
Åsa KeitaDepartment of Biomedical and Clinical Sciences, Linköping University, Linköping, Sweden.
Henrik HjortswangDepartment of Clinical and Experimental Science, Linköping University, Linköping, Sweden.
Johan SöderholmDepartment of Biomedical and Clinical Sciences, Linköping University, Linköping, Sweden.
Johanna SundinDepartment of Internal Medicine & Clinical Nutrition, Institute of Medicine, Sahlgrenska Academy, Gothenburg, Sweden.
Hans TörnblomDepartment of Molecular and Clinical Medicine, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Magnus SimrénDepartment of Molecular and Clinical Medicine, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Hans StridDepartment of Internal Medicine, Södra Älvsborg Hospital, Borås, Sweden.
Maria K MagnussonDepartment of Microbiology and Immunology, Institute of Biomedicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Lena ÖhmanDepartment of Microbiology and Immunology, Institute of Biomedicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Örebro University · SEUniversity of Gothenburg · SELinköping University · SEKarolinska Institutet · SEUppsala University · SEIkerbasque · ESKarolinska University Hospital · SESödra Älvsborg Hospital · SEUniversity of North Carolina at Chapel Hill · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Improved mucosal immune profiling in active and quiescent colonic inflammatory bowel disease (IBD) is needed to develop therapeutic options for treating and preventing flares. This study therefore aimed to provide a comprehensive mucosal characterization with emphasis on immunological host response of patients with active ulcerative colitis (UC active), UC during remission (UC remission) and active colonic Crohn's disease (CD active). Methods: Colonic biopsies from 47 study subjects were collected for gene expression and pathway analyses using the NanoString host-response panel, including 776 genes and 56 immune-related pathways. Results: The majority of mucosal gene expression and signaling pathway scores were increased in active IBD (n=27) compared to healthy subjects (n=10). However, both active IBD and UC remission (n=10) demonstrated decreased gene expression and signaling pathway scores related to autophagy, alpha kinase-1 and IL-17 signaling pathways compared to healthy subjects. Further, UC remission was characterized by decreased scores of several signaling pathways linked to homeostasis along with increased mononuclear cell migration pathway score as compared to healthy subjects. No major differences in the colonic mucosal gene expression between CD active (n=7) and UC (n=20) active were observed. Conclusion: This study indicates that autophagy, alpha kinase-1 and IL-17 signaling pathways are persistently downregulated in UC irrespective of disease activity. Further, UC patients in remission present a unique mucosal environment, potentially preventing patients from reaching and sustaining true homeostasis. These findings may enable better comprehension of the remitting and relapsing pattern of colonic IBD and guide future treatment and prevention of flares.

Indexed as

gene expressionhomeostasishost responseinflammatory bowel diseasesmucosal transcriptome

Identifiers

PMID35928254
PMCPMC9343467
OpenAlexW4288069747

What OpenQuestion holds

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Registered trials

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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.