Evidence map›Paper›PMID 26732677›Full record

ArticleMucosal immunology2016

Neutrophil interactions with epithelial-expressed ICAM-1 enhances intestinal mucosal wound healing.

R Sumagin, J C Brazil, P Nava, H Nishio, A Alam, A C Luissint, D A Weber, A S Neish, A Nusrat, C A Parkos

Open access · bronzeAbstract read
In one paragraph

Article in Mucosal immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.

0numbers the graph read from it
0cells of the map it votes in
73citing papers in PubMed
7.3field-weighted citation impact, top 2% 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

73 citing papers in PubMed, 102 citations in OpenAlex.

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  20. Review

13 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

10 authors at 4 institutions in 2 countries.

R SumaginDepartment of Pathology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, USA.
J C BrazilDepartment of Pathology, University of Michigan Medical School, Ann Arbor, Michigan, USA.
P NavaDepartamento de Fisiología, Biofísica y Neurociencias, Centro de Investigación y de Estudios Avanzados, Instituto Politécnico Nacional, Mexico, Mexico.
H NishioDepartment of Pathology, Emory University School of Medicine, Atlanta, Georgia, USA.
A AlamDepartment of Pathology, Emory University School of Medicine, Atlanta, Georgia, USA.
A C LuissintDepartment of Pathology, University of Michigan Medical School, Ann Arbor, Michigan, USA.
D A WeberDepartment of Pathology, Emory University School of Medicine, Atlanta, Georgia, USA.
A S NeishDepartment of Pathology, Emory University School of Medicine, Atlanta, Georgia, USA.
A NusratDepartment of Pathology, University of Michigan Medical School, Ann Arbor, Michigan, USA.
C A ParkosDepartment of Pathology, University of Michigan Medical School, Ann Arbor, Michigan, USA.
Emory University · USUniversity of Michigan · USInstituto Politécnico Nacional · MXNorthwestern University · US

Funding

University of Michigan Center for Gastrointestinal ResearchP30DK034933 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI WILEY, JOHN W · 1986 to 2021
$22.5M
Regulation of intestinal epithelial barrier function by intercellular junction proteins in health and diseaseR01DK059888 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI ASMA NUSRAT · 2001 to 2026
$10.5M
Intestinal Mucosal Wound Resealing in IBDR01DK055679 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI ASMA NUSRAT · 2004 to 2026
$8.1M
Intestinal Inflammation: Signaling proteins and the rate of PMN transmigrationR01DK079392 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI PARKOS, CHARLES A · 2007 to 2025
$7.2M
Neutrophil Interactions with Intestinal Epithelial CellsR01DK072564 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI PARKOS, CHARLES A · 2005 to 2020
$6.5M
Structure-Function Studies on Intestinal Epithelial JAMR01DK061379 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI PARKOS, CHARLES A · 2002 to 2021
$6.3M
Emory Epithelial Pathobiology Research Development CenterR24DK064399 · NIDDK · EMORY UNIVERSITY · PI PARKOS, CHARLES A · 2003 to 2012
$5.3M
Formyl peptide receptors as mediators of intestinal mucosal homeostasisR01DK089763 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI NEISH, ANDREW S, NUSRAT, ASMA · 2011 to 2020
$4.7M
Control of Epithelial Proliferation by the MicrobiotaR01CA179424 · NCI · EMORY UNIVERSITY · PI JONES, RHEINALLT MELFYN, NEISH, ANDREW S · 2014 to 2017
$1.3M
Neutrophil interactions with apical ICAM-1 regulate intestinal epithelial homeostK01DK101675 · NIDDK · NORTHWESTERN UNIVERSITY AT CHICAGO · PI SUMAGIN, RONEN · 2014 to 2018
$710k
Microbially generated protons mediate interkingdom host-microbiome cross-talk and maintain intestinal homeostasis via reciprocal functions of two proton-sensing GPCRsK01DK114391 · NIDDK · UNIVERSITY OF KENTUCKY · PI ALAM, M. ASHFAQUL · 2017 to 2021
$530k
INTESTINAL MUCOSAL WOUND RESEALING IN SURGICAL DISEASESR29DK055679 · NIDDK · EMORY UNIVERSITY · PI NUSRAT, ASMA · 1998 to 2002
$324k
NCI NIH HHS R01 CA179424NIDDK NIH HHS K01 DK101675NIDDK NIH HHS K01 DK114391NIDDK NIH HHS P30 DK034933NIDDK NIH HHS R01 DK055679NIDDK NIH HHS R01 DK059888NIDDK NIH HHS R01 DK061379NIDDK NIH HHS R01 DK072564NIDDK NIH HHS R01 DK079392NIDDK NIH HHS R01 DK089763NIDDK NIH HHS R24 DK064399NIDDK NIH HHS R29 DK055679
6 · The paper itself

Abstract

A characteristic feature of gastrointestinal tract inflammatory disorders, such as inflammatory bowel disease, is polymorphonuclear neutrophil (PMN) transepithelial migration (TEM) and accumulation in the gut lumen. PMN accumulation within the intestinal mucosa contributes to tissue injury. Although epithelial infiltration by large numbers of PMNs results in mucosal injury, we found that PMN interactions with luminal epithelial membrane receptors may also play a role in wound healing. Intercellular adhesion molecule-1 (ICAM-1) is a PMN ligand that is upregulated on apical surfaces of intestinal epithelial cells under inflammatory conditions. In our study, increased expression of ICAM-1 resulted in enhanced PMN binding to the apical epithelium, which was associated with reduced PMN apoptosis. Following TEM, PMN adhesion to ICAM-1 resulted in activation of Akt and β-catenin signaling, increased epithelial-cell proliferation, and wound healing. Such responses were ICAM-1 dependent as engagement of epithelial ICAM-1 by antibody-mediated cross-linking yielded similar results. Furthermore, using an in-vivo biopsy-based, colonic-mucosal-injury model, we demonstrated epithelial ICAM-1 has an important role in activation of epithelial Akt and β-catenin signaling and wound healing. These findings suggest that post-migrated PMNs within the intestinal lumen can regulate epithelial homeostasis, thereby identifying ICAM-1 as a potential therapeutic target for promoting mucosal wound healing.

Indexed as

Immunity, MucosalAnimalsbeta CateninBiopsyCell CommunicationCell LineCell ProliferationColonEpithelial CellsGene Expression RegulationHumansIntercellular Adhesion Molecule-1Intestinal MucosaMaleMiceMice, Inbred C57BLbeta CateninCTNNB1 protein, mouseIntercellular Adhesion Molecule-1Proto-Oncogene Proteins c-akt

Identifiers

PMID26732677
PMCPMC4935657
OpenAlexW2224132120

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.