Evidence map›Paper›PMID 34603288›Full record

ArticleFrontiers in immunology2021

Formyl Peptide Receptors and Annexin A1: Complementary Mechanisms to Infliximab in Murine Experimental Colitis and Crohn's Disease.

Marina de Paula-Silva, Gustavo Henrique Oliveira da Rocha, Milena Fronza Broering, Maria Luíza Queiroz, Silvana Sandri, Rodrigo Azevedo Loiola, Sonia Maria Oliani, Andrea Vieira, Mauro Perretti, Sandra Helena Poliselli Farsky

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

12 citing papers in PubMed, 28 citations in OpenAlex.

  1. RNF168 promotes chronic colitis through ANXA7-mediated autophagy and NLRP3-driven pyroptosis.Apoptosis : an international journal on programmed cell death · 2026
    Article
  2. Crotoxin fromFrontiers in immunology · 2026
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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

10 authors at 4 institutions in 2 countries.

Marina de Paula-SilvaDepartment of Clinical and Toxicological Analyses, University of São Paulo (USP), São Paulo, Brazil.
Gustavo Henrique Oliveira da RochaDepartment of Clinical and Toxicological Analyses, University of São Paulo (USP), São Paulo, Brazil.
Milena Fronza BroeringDepartment of Clinical and Toxicological Analyses, University of São Paulo (USP), São Paulo, Brazil.
Maria Luíza QueirozGastroenterology Service, Irmandade da Santa Casa de Misericórdia de São Paulo, São Paulo, Brazil.
Silvana SandriDepartment of Clinical and Toxicological Analyses, University of São Paulo (USP), São Paulo, Brazil.
Rodrigo Azevedo LoiolaDepartment of Clinical and Toxicological Analyses, University of São Paulo (USP), São Paulo, Brazil.
Sonia Maria OlianiDepartment of Biology, São Paulo State University (UNESP), São José do Rio Preto, São Paulo, Brazil.
Andrea VieiraGastroenterology Service, Irmandade da Santa Casa de Misericórdia de São Paulo, São Paulo, Brazil.
Mauro PerrettiCentre for Biochemical Pharmacology, The William Harvey Research Institute, Barts and The London School of Medicine, Queen Mary University of London (QMUL), London, United Kingdom.
Sandra Helena Poliselli FarskyDepartment of Clinical and Toxicological Analyses, University of São Paulo (USP), São Paulo, Brazil.
Universidade de São Paulo · BRIrmandade da Santa Casa de Misericórdia de São Paulo · BRQueen Mary University of London · GBUniversidade Estadual Paulista (Unesp) · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Non-responsiveness to anti-TNF-α therapies presents relevant rates in inflammatory bowel disease patients, presenting the need to find biomarkers involved in therapeutic efficacy. Herein, we demonstrate that higher levels of colonic formyl peptide receptor 1 and annexin A1 correlate with histological recovery in Crohn's disease patients under remission. Using the dextran sulfate sodium colitis model in mice, we suggest that infliximab induces annexin A1 expression and secretion in activated intestinal leukocytes. Conversely, this mechanism might stimulate epithelial formyl peptide receptors, inducing wound healing and consequent histological remission. Our data indicate that assessing intestinal expressions of formyl peptide receptors and annexin A1 might provide precious information on the disease activity and responsiveness to infliximab in inflammatory bowel disease patients.

Indexed as

AdultAnimalsAnnexin A1Antirheumatic AgentsBiopsyColitisCrohn DiseaseDisease Models, AnimalDisease SusceptibilityFemaleHumansInfliximabLeukocytesMaleMiceMice, KnockoutAnnexin A1Antirheumatic AgentsInfliximabReceptors, Formyl PeptideTumor Necrosis Factor Inhibitorsannexin A1biomarkersCrohn’s diseasedextran sodium sulfateformyl peptide receptorinfliximab

Identifiers

PMID34603288
PMCPMC8484756
OpenAlexW3201393771

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.