Evidence map›Paper›PMID 26687991›Full record

ArticleThe American journal of pathology2016

Targeting of Neutrophil Lewis X Blocks Transepithelial Migration and Increases Phagocytosis and Degranulation.

Jennifer C Brazil, Ronen Sumagin, Richard D Cummings, Nancy A Louis, Charles A Parkos

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

24 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. Review
  8. Review
  9. Article
  10. Review
  11. LEUKOCYTE-EPITHELIAL INTERACTIONS: A DOUBLE-EDGED SWORD THAT PROTECTS AND INJURES DURING HEALTH AND DISEASE.Transactions of the American Clinical and Climatological Association · 2022
    Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Regulation of neutrophil function by selective targeting of glycan epitopes expressed on the integrin CD11b/CD18.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020
    Article
  17. Review
  18. Article
  19. Review
  20. Article
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 2 institutions in 1 country.

Jennifer C BrazilDepartment of Pathology and Laboratory Medicine, Emory University, Atlanta, Georgia; Department of Pathology, University of Michigan, Ann Arbor, Michigan. Electronic address: brazilj@med.umich.edu.
Ronen SumaginDepartment of Pathology and Laboratory Medicine, Emory University, Atlanta, Georgia; Department of Pathology, Northwestern University, Chicago, Illinois.
Richard D CummingsDepartment of Biochemistry, Emory University, Atlanta, Georgia.
Nancy A LouisDepartment of Neonatal-Perinatal Medicine, Emory University, Atlanta, Georgia.
Charles A ParkosDepartment of Pathology and Laboratory Medicine, Emory University, Atlanta, Georgia; Department of Pathology, University of Michigan, Ann Arbor, Michigan. Electronic address: cparkos@med.umich.edu.
Emory University · USUniversity of Michigan–Ann Arbor · US

Funding

Tumor Environment and Metastasis (TEAM) Research ProgramP30CA060553 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI Daniela E Matei · 1993 to 2026
$153.9M
Protein-glycan Interactions in the Vascular SystemP01HL085607 · NHLBI · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI MCEVER, RODGER PAUL · 2006 to 2015
$16.8M
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
Overall Priority Score P41GM103694 · NIGMS · EMORY UNIVERSITY · PI CUMMINGS, RICHARD D · 2013 to 2018
$6.9M
Neutrophil Interactions with Intestinal Epithelial CellsR01DK072564 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI PARKOS, CHARLES A · 2005 to 2020
$6.5M
Neutrophil interactions with apical ICAM-1 regulate intestinal epithelial homeostK01DK101675 · NIDDK · NORTHWESTERN UNIVERSITY AT CHICAGO · PI SUMAGIN, RONEN · 2014 to 2018
$710k
FEI Transmission Electron Microscope with Tomography CapabilityS10RR025679 · NCRR · EMORY UNIVERSITY · PI SPEARMAN, PAUL W. · 2009 to 2009
$500k
NCI NIH HHS P30 CA060553NCRR NIH HHS S10 RR025679NCRR NIH HHS S10 RR025679 01NHLBI NIH HHS HL085607NHLBI NIH HHS P01 HL085607NIDDK NIH HHS DK072564NIDDK NIH HHS DK079392NIDDK NIH HHS K01 DK101675NIDDK NIH HHS R01 DK072564NIDDK NIH HHS R01 DK079392NIGMS NIH HHS P41 GM103694NIGMS NIH HHS P41GM103694
6 · The paper itself

Abstract

Polymorphonuclear leukocytes (PMNs) are innate immune cells whose principal function is to migrate from the blood to sites of inflammation, where they exert crucial anti-infectious and immunomodulatory effects. However, dysregulated migration of PMNs into mucosal epithelial tissues is characteristic of chronic inflammatory disorders, including inflammatory bowel disease. Carbohydrate-mediated binding interactions between PMN Lewis glycans and endothelial glycan-binding proteins are critical for initial migration of PMN out of the vasculature. However, the role of Lewis glycans during transepithelial migration (TEM) has not been well characterized. Herein, we show that antibody blockade of Lewis X (Le(x)) displayed as terminal glycan residues on the PMN surface blocks chemotaxis and TEM while enhancing PMN-adhesive interactions with intestinal epithelia. Unexpectedly, targeting of subterminal Le(x) residues within glycan chains had no effect on PMN migration or adhesive interactions. There was increased surface expression of Le(x) on PMN after TEM, and blockade of terminal Le(x) regulated post-migratory PMN functions, increasing PMN phagocytosis and the surface mobilization of azurophilic (CD63, myeloperoxidase, and neutrophil elastase) and specific (CD66b and lactoferrin) granule markers. These findings suggest that terminal Le(x) represents a potential target for regulating PMN trafficking and function in inflamed mucosa. Furthermore, given its abundant expression on migrating PMN, Le(x) may be a rational target for modulating inflammation in diseases where dysregulated PMN influx is associated with host tissue damage.

Indexed as

Cell AdhesionCells, CulturedChemotaxisEpitheliumHumansInflammatory Bowel DiseasesIntestinal MucosaLewis X AntigenNeutrophilsPhagocytosisTransendothelial and Transepithelial MigrationLewis X Antigen

Identifiers

PMID26687991
PMCPMC4729268
OpenAlexW2245271398

What OpenQuestion holds

Textmetadata
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.