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Updated: May 19, 2026

Bioparticle Microarrays for Chemotactic and Molecular Analysis of Human Neutrophil Swarming in vitro

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Published on: February 16, 2020

Galectin-1 promotes human neutrophil migration.

Constance Auvynet¹, Samadhi Moreno, Erika Melchy

¹Departamento de Medicina Molecular y Bioprocesos, Instituto de Biotecnologia, Universidad Nacional Autónoma de México, Avenida Universidad 2001, Col Chamilpa, Cuernavaca, Morelos 62210, Mexico.

|September 4, 2012

Summary

Galectin-1 (Gal-1) can surprisingly attract neutrophils, a key part of innate immunity, to injury sites. This novel chemoattractant function, mediated by CD43, contrasts with its previously known anti-inflammatory roles.

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Area of Science:

Immunology
Molecular Biology
Cell Biology

Background:

Innate immune response involves neutrophil recruitment via chemotactic molecules.
Galectins, including galectin-3 and -9, modulate inflammation and cell migration.
Galectin-1 (Gal-1) was traditionally viewed as anti-inflammatory, inhibiting polymorphonuclear leukocyte (PMN) influx.

Purpose of the Study:

To investigate the effect of Gal-1 on neutrophil recruitment independently of other inflammatory stimuli.
To elucidate the mechanism by which Gal-1 influences neutrophil migration.

Main Methods:

In vitro and in vivo assays were used to assess neutrophil migration.
Investigated the role of G-protein-coupled receptors, CD43, and the p38 MAPK pathway.

Main Results:

Galectin-1 demonstrated the capacity to induce neutrophil migration both in vitro and in vivo.
This migration was not mediated by G-protein-coupled receptors.
The effect appears to involve the sialoglycoprotein CD43 and the p38 mitogen-activated protein kinase pathway.

Conclusions:

Galectin-1 exhibits a novel chemoattractant function for neutrophils.
This function is potentially mediated through CD43 binding and the p38 MAPK pathway.
Gal-1's role is context-dependent, acting as either a chemoattractant or an inhibitor of migration, highlighting its potential as a drug development target.