Evidence map›Paper›PMID 36675038›Full record

ReviewInternational journal of molecular sciences2023

Pathophysiology of Inflammatory Bowel Disease: Innate Immune System.

Angela Saez, Beatriz Herrero-Fernandez, Raquel Gomez-Bris, Hector Sánchez-Martinez, Jose M Gonzalez-Granado

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 294 papers, 8 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
294citing papers in PubMed, 8 pooled it
77.8field-weighted citation impact, top 1% 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

294 citing papers in PubMed, 8 syntheses or guidelines pooled it, 473 citations in OpenAlex.

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  4. Short-chain fatty acids in the treatment of ulcerative colitis. Systematic review and meta-analysis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
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234 more citing papers are in PubMed but not listed here.

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

5 authors at 3 institutions in 1 country.

Angela SaezLamImSys Lab, Instituto de Investigación Sanitaria Hospital 12 de Octubre (imas12), 28041 Madrid, Spain.ORCID 0000-0002-9189-4737
Beatriz Herrero-FernandezLamImSys Lab, Instituto de Investigación Sanitaria Hospital 12 de Octubre (imas12), 28041 Madrid, Spain.
Raquel Gomez-BrisLamImSys Lab, Instituto de Investigación Sanitaria Hospital 12 de Octubre (imas12), 28041 Madrid, Spain.ORCID 0000-0001-6665-7732
Hector Sánchez-MartinezLamImSys Lab, Instituto de Investigación Sanitaria Hospital 12 de Octubre (imas12), 28041 Madrid, Spain.
Jose M Gonzalez-GranadoLamImSys Lab, Instituto de Investigación Sanitaria Hospital 12 de Octubre (imas12), 28041 Madrid, Spain.ORCID 0000-0002-1177-869X
Research Institute Hospital 12 de Octubre · ESUniversidad Complutense de Madrid · ESUniversidad Francisco de Vitoria · ES

Funding

Comunidad de Madrid PEJ-2020-TL/BMD-17604Instituto de Salud Carlos III PI20/00306Ministerio de Ciencia, Innovación y Universidades (MCNU) FPU18/00895Ministerio de Ciencia, Innovación y Universidades (MCNU) FPU19/01774
6 · The paper itself

Abstract

Inflammatory bowel disease (IBD), comprising Crohn's disease (CD) and ulcerative colitis (UC), is a heterogeneous state of chronic intestinal inflammation with no exact known cause. Intestinal innate immunity is enacted by neutrophils, monocytes, macrophages, and dendritic cells (DCs), and innate lymphoid cells and NK cells, characterized by their capacity to produce a rapid and nonspecific reaction as a first-line response. Innate immune cells (IIC) defend against pathogens and excessive entry of intestinal microorganisms, while preserving immune tolerance to resident intestinal microbiota. Changes to this equilibrium are linked to intestinal inflammation in the gut and IBD. IICs mediate host defense responses, inflammation, and tissue healing by producing cytokines and chemokines, activating the complement cascade and phagocytosis, or presenting antigens to activate the adaptive immune response. IICs exert important functions that promote or ameliorate the cellular and molecular mechanisms that underlie and sustain IBD. A comprehensive understanding of the mechanisms underlying these clinical manifestations will be important for developing therapies targeting the innate immune system in IBD patients. This review examines the complex roles of and interactions among IICs, and their interactions with other immune and non-immune cells in homeostasis and pathological conditions.

Indexed as

Immunity, InnateInflammatory Bowel DiseasesHumansImmune SystemInflammationIntestinal MucosaLymphocytesCrohn’s diseasedendritic cellinflammatory bowel diseaseinnate immune systemintestinal homeostasismacrophageneutrophilulcerative colitis

Identifiers

PMID36675038
PMCPMC9863490
OpenAlexW4315797293

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.