Evidence map›Paper›PMID 24130820›Full record

ArticlePloS one2013

Dysregulation of anti-inflammatory annexin A1 expression in progressive Crohns Disease.

Angela Sena, Irina Grishina, Anne Thai, Larissa Goulart, Monica Macal, Anne Fenton, Jay Li, Thomas Prindiville, Sonia Maria Oliani, Satya Dandekar and 2 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
4.0field-weighted citation impact, top 6% 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

33 citing papers in PubMed, 95 citations in OpenAlex.

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  19. Reduced Annexin A3 in schizophrenia.European archives of psychiatry and clinical neuroscience · 2020
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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

12 authors at 3 institutions in 2 countries.

Angela SenaDepartment of Medical Microbiology and Immunology, University of California Davis, Davis, California, United States of America ; Nanobiotechnology Laboratory, Institute of Genetics and Biochemistry, Federal University of Uberlandia, Uberlandia, Minas Gerais, Brazil.
Irina Grishina
Anne Thai
Larissa Goulart
Monica Macal
Anne Fenton
Jay Li
Thomas Prindiville
Sonia Maria Oliani
Satya Dandekar
Luiz Goulart
Sumathi Sankaran-Walters
University of California, Davis · USUniversidade Estadual Paulista (Unesp) · BRUniversidade Federal de Uberlândia · BR

Funding

National Institute on Aging (NIA) ColonyP51OD011107 · OD · UNIVERSITY OF CALIFORNIA AT DAVIS · PI Simon J. Atkinson · 2012 to 2026
$191.5M
Building Interdisciplinary Research Careers in Womens Health at UC Davis - Administrative SupplementK12HD051958 · NICHD · UNIVERSITY OF CALIFORNIA DAVIS · PI LANE, NANCY E · 2005 to 2023
$9.6M
INTESTINAL CYTOKINE &TCELL HOMEOSTASIS IN SIV INFECTIONR01AI043274 · NIAID · UNIVERSITY OF CALIFORNIA DAVIS · PI DANDEKAR, SATYA · 1998 to 2013
$5.1M
HIV reservoir and CD4 repopulation in gut lymphoid tissueR01DK061297 · NIDDK · UNIVERSITY OF CALIFORNIA DAVIS · PI DANDEKAR, SATYA · 2002 to 2012
$3.5M
NIAID NIH HHS AI43274NIAID NIH HHS R01 AI043274NICHD NIH HHS K12 HD051958NIDDK NIH HHS R01 DK061297NIDDK NIH HHS R01 DK61297NIH HHS P51 OD011107
6 · The paper itself

Abstract

backgroundDevelopment of inflammatory bowel disease (IBD) involves the interplay of environmental and genetic factors with the host immune system. Mechanisms contributing to immune dysregulation in IBD are not fully defined. Development of novel therapeutic strategies is focused on controlling aberrant immune response in IBD. Current IBD therapy utilizes a combination of immunomodulators and biologics to suppress pro-inflammatory effectors of IBD. However, the role of immunomodulatory factors such as annexin A1 (ANXA1) is not well understood. The goal of this study was to examine the association between ANXA1 and IBD, and the effects of anti-TNF-α, Infliximab (IFX), therapy on ANXA1 expression.

methodsANXA1 and TNF-α transcript levels in PBMC were measured by RT PCR. Clinical follow up included the administration of serial ibdQs. ANXA1 expression in the gut mucosa was measured by IHC. Plasma ANXA1 levels were measured by ELISA.

resultsWe found that the reduction in ANXA1 protein levels in plasma coincided with a decrease in the ANXA1 mRNA expression in peripheral blood of IBD patients. ANXA1 expression is upregulated during IFX therapy in patients with a successful intervention but not in clinical non-responders. The IFX therapy also modified the cellular immune activation in the peripheral blood of IBD patients. Decreased expression of ANXA1 was detected in the colonic mucosa of IBD patients with incomplete resolution of inflammation during continuous therapy, which correlated with increased levels of TNF-α transcripts. Gut mucosal epithelial barrier disruption was evident by increased plasma bacterial 16S levels.

conclusionLoss of ANXA1 expression may support inflammation during IBD and can serve as a biomarker of disease progression. Changes in ANXA1 levels may be predictive of therapeutic efficacy.

Indexed as

Disease ProgressionGene Expression RegulationAdultAgedAnnexin A1Antibodies, MonoclonalCrohn DiseaseDNA, BacterialDNA, RibosomalFemaleHumansInflammationInfliximabIntestinal MucosaLymphocyte ActivationMaleAnnexin A1Antibodies, MonoclonalDNA, BacterialDNA, RibosomalInfliximabRNA, MessengerTumor Necrosis Factor-alpha

Identifiers

PMID24130820
PMCPMC3794972
OpenAlexW1974525742

What OpenQuestion holds

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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.