Evidence map›Paper›PMID 31585707›Full record

ArticleBiophysical journal2019

Human Neutrophils Will Crawl Upstream on ICAM-1 If Mac-1 Is Blocked.

Alexander Buffone, Nicholas R Anderson, Daniel A Hammer

Open access · bronzeAbstract read
In one paragraph

Article in Biophysical journal, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

28 citing papers in PubMed, 43 citations in OpenAlex.

  1. Review
  2. Probing the Mechano-Redox Control of Cell Movement Using Microfluidic Assays.Methods in molecular biology (Clifton, N.J.) · 2026
    Article
  3. Article
  4. Review
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  6. Article
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  10. Modeling Brain Vasculature Immune Interactions In Vitro.Cold Spring Harbor perspectives in medicine · 2023
    Review
  11. Observational
  12. Review
  13. Keratocytes migrate against flow with a roly-poly-like mechanism.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  14. Review
  15. Article
  16. Article
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  20. Review
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

3 authors at 1 institution in 1 country.

Alexander BuffoneDepartments of Chemical and Biomolecular Engineering, University of Pennsylvania, Philadelphia, Pennsylvania; Bioengineering, University of Pennsylvania, Philadelphia, Pennsylvania.
Nicholas R AndersonDepartments of Chemical and Biomolecular Engineering, University of Pennsylvania, Philadelphia, Pennsylvania.
Daniel A HammerDepartments of Chemical and Biomolecular Engineering, University of Pennsylvania, Philadelphia, Pennsylvania; Bioengineering, University of Pennsylvania, Philadelphia, Pennsylvania. Electronic address: hammer@seas.upenn.edu.
University of Pennsylvania · US

Funding

The mechanochemical control of T-cell directional migration under flowR01GM123019 · NIGMS · UNIVERSITY OF PENNSYLVANIA · PI HAMMER, DANIEL A · 2017 to 2020
$1.7M
Controlling the Upstream Migration of Neutrophils through the Modulation of Mac-1R21GM133060 · NIGMS · UNIVERSITY OF PENNSYLVANIA · PI HAMMER, DANIEL A · 2019 to 2020
$439k
NIGMS NIH HHS R01 GM123019NIGMS NIH HHS R21 GM133060
6 · The paper itself

Abstract

The recruitment of neutrophils to sites of inflammatory insult is a hallmark of the innate immune response. Neutrophil recruitment is regulated by a multistep process that includes cell rolling, activation, adhesion, and transmigration through the endothelium commonly referred to as the leukocyte adhesion cascade. After selectin-mediated braking, neutrophils migrate along the activated vascular endothelium on which ligands, including intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1), are expressed. Previous studies have shown that two cells that commonly home from blood vessel to tissue-T cells and hematopoietic stem and progenitor cells-use the integrin lymphocyte functional antigen-1 (LFA-1) to migrate against the direction of shear flow once adherent on ICAM-1 surfaces. Like T cells and hematopoietic stem and progenitor cells, neutrophils express LFA-1, but they also express macrophage-1 antigen (Mac-1), which binds to ICAM-1. Previous reports have shown that neutrophils will not migrate against the direction of flow on ICAM-1, but we hypothesized this was due to the influence of Mac-1. Here, we report that both the HL-60 neutrophil-like cell line and primary human neutrophils can migrate against the direction of fluid flow on ICAM-1 surfaces via LFA-1 if Mac-1 is blocked; otherwise, they migrate downstream. We demonstrate this both on ICAM-1 surfaces and on activated endothelium. In sum, both LFA-1 and Mac-1 binding ICAM-1 play a critical role in determining the direction of neutrophil migration along the endothelium, and their interaction may play an important role in controlling neutrophil trafficking during inflammation.

Indexed as

Cell MovementAntibodies, NeutralizingCell Line, TumorCells, CulturedHumansHuman Umbilical Vein Endothelial CellsIntercellular Adhesion Molecule-1Lymphocyte Function-Associated Antigen-1Macrophage-1 AntigenNeutrophilsAntibodies, NeutralizingIntercellular Adhesion Molecule-1Lymphocyte Function-Associated Antigen-1Macrophage-1 Antigen

Identifiers

PMID31585707
PMCPMC6817642
OpenAlexW2974068600

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.