Evidence map›Paper›PMID 11413108›Full record

ArticleGut2001

Decreased Bax expression by mucosal T cells favours resistance to apoptosis in Crohn's disease.

J Itoh, C de La Motte, S A Strong, A D Levine, C Fiocchi

Registry-linked trialOpen access · bronzeAbstract read
In one paragraph

Article in Gut, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT00561548 (Impact of Anti-TNF Antibodies on the T-lymphocyte and Macrophage Cooperation in the Crohn Disease), which is not on this map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
2.8field-weighted citation impact, top 9% 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.

NCT00561548 naterminatednot on this mapstarted 2007, after this paper: background citation

Impact of Anti-TNF Antibodies on the T-lymphocyte and Macrophage Cooperation in the Crohn Disease

TypeinterventionalSponsorCentre Hospitalier Universitaire de NiceRan2007 to 2009Enrolled20ConditionsCrohn DiseaseArmsrectosigmoïdal biopsies
3 · Its place in the literature

Who cites it

46 citing papers in PubMed, 132 citations in OpenAlex.

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  8. Emerging Pathological Engagement of Ferroptosis in Gut Diseases.Oxidative medicine and cellular longevity · 2021
    Review
  9. Suppression of Inflammatory Cytokines Expression with Bitter Melon (Journal of translational internal medicine · 2020
    Article
  10. Article
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  19. Role of DOR-β-arrestin1-Bcl2 signal transduction pathway and intervention effects of oxymatrine in ulcerative colitis.Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban · 2014
    Article
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

J ItohDivision of Gastroenterology, University Hospitals of Cleveland, Case Western Reserve University School of Medicine, Cleveland, Ohio 44106, USA.
C de La Motte
S A Strong
A D Levine
C Fiocchi
Case Western Reserve University · US

Funding

MUCOSAL LYMPHOKINES IN INFLAMMATORY BOWEL DISEASER37DK030399 · NIDDK · CLEVELAND CLINIC LERNER COM-CWRU · PI FIOCCHI, CLAUDIO · 1999 to 2008
$3.2M
Cell interactions in the inflammed intestinal mucosaR01DK050984 · NIDDK · CLEVELAND CLINIC LERNER COM-CWRU · PI FIOCCHI, CLAUDIO · 1995 to 2014
$3.1M
The Extracellular Matrix Inflammatory Bowel DiseaseR01DK054213 · NIDDK · CASE WESTERN RESERVE UNIVERSITY · PI LEVINE, ALAN DAVID · 1998 to 2010
$2.8M
DETACHMENT INDUCED APOPTOSIS IN INTESTINAL EPITHELIUMR01CA077717 · NCI · CASE WESTERN RESERVE UNIVERSITY · PI LEVINE, ALAN DAVID · 1999 to 2003
$1.4M
MUCOSAL LYMPHOKINES IN INFLAMMATORY BOWEL DISEASER01DK030399 · NIDDK · CLEVELAND CLINIC FOUNDATION · PI FIOCCHI, CLAUDIO · 1986 to 1997
–
NCI NIH HHS CA77717NIDDK NIH HHS DK30399NIDDK NIH HHS DK50984NIDDK NIH HHS DK54213
6 · The paper itself

Abstract

backgroundActivated T cells are more susceptible to apoptosis than resting T cells. As intestinal T cells normally exhibit a higher state of activation, increased apoptosis may be necessary to maintain immune homeostasis in the specialised microenvironment of the mucosa. On the other hand, in Crohn's disease (CD) mucosal T cells are resistant to apoptosis, suggesting abnormal regulation of cell death mechanisms.

aimsTo investigate differences in expression of anti- and proapoptotic Bcl-2 family proteins, key regulators of apoptosis, between circulating and mucosal T cells, and possible alterations in CD. PATIENTS AND

methodsLamina propria T cells (LPT) were isolated from 10 control, seven CD, and eight ulcerative colitis (UC) patients, and peripheral blood T cells (PBT) from healthy volunteers. Purified T cells were stained intracellularly for Bcl-2, Bcl-x(L), and Bax, and mean fluorescence intensity measured by flow cytometry.

resultsCompared with PBT, the expression level of Bcl-2 and Bax, but not Bcl-x(L), was significantly greater in LPT, resulting in lower Bcl-x(L)/Bax ratios. In PBT, Bax expression was highly and significantly correlated with both Bcl-2 and Bcl-x(L), but correlation with Bcl-2 was absent in LPT. Bax expression in CD, but not UC, LPT was significantly lower than in control LPT, resulting in a significantly higher Bcl-x(L)/Bax ratio. The significant correlation of Bcl-x(L) to Bax was preserved in CD, but not UC, LPT.

conclusionsRegulation of Bcl-2 family protein expression differs between circulating and mucosal T cells, probably underlying diverse survival potentials. In CD LPT, a low Bax expression and a high Bcl-x(L)/Bax ratio favour resistance to apoptosis and may contribute to the chronicity of inflammation.

Indexed as

AdolescentAdultAgedAged, 80 and overApoptosisbcl-2-Associated X ProteinCase-Control StudiesColitis, UlcerativeCrohn DiseaseFemaleFlow CytometryHumansImmunity, CellularIntestinal MucosaMaleMiddle AgedBAX protein, humanbcl-2-Associated X ProteinProto-Oncogene ProteinsProto-Oncogene Proteins c-bcl-2

Identifiers

PMID11413108
PMCPMC1728348
OpenAlexW2134090681

What OpenQuestion holds

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Registered trials

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.