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Related Experiment Video

Updated: May 12, 2026

Three-Dimensional Cell Culture Models to Investigate the Epithelial Barrier in Eosinophilic Esophagitis

Three-Dimensional Cell Culture Models to Investigate the Epithelial Barrier in Eosinophilic Esophagitis

Published on: May 10, 2024

Eosinophil-expressed galectin-3 regulates cell trafficking and migration.

Xiao Na Ge¹, Sung Gil Ha, Fu-Tong Liu

¹Department of Veterinary and Biomedical Sciences, University of Minnesota St. Paul, MN, USA.

Frontiers in Pharmacology

|April 12, 2013

Summary

Galectin-3 (Gal-3) is crucial for eosinophil (Eos) trafficking and migration in allergic airway inflammation. Mice lacking Gal-3 show reduced Eos recruitment and impaired cell adhesion and migration, highlighting Gal-3

Keywords:

allergic airway inflammation cell trafficking eosinophils galectin-3 migration

Related Experiment Videos

Last Updated: May 12, 2026

Three-Dimensional Cell Culture Models to Investigate the Epithelial Barrier in Eosinophilic Esophagitis

Three-Dimensional Cell Culture Models to Investigate the Epithelial Barrier in Eosinophilic Esophagitis

Published on: May 10, 2024

Area of Science:

Immunology
Allergy and Asthma Research
Cellular and Molecular Biology

Background:

Galectin-3 (Gal-3) is involved in allergic airway inflammation.
Gal-3-deficient mice show reduced eosinophil (Eos) recruitment to the airways.
Gal-3 can function intracellularly and extracellularly.

Purpose of the Study:

To investigate the role of Eos-expressed Gal-3 in Eos trafficking and migration during allergic airway inflammation.
To use bone marrow-derived Eos from wild-type (WT) and Gal-3-deficient mice for in vitro studies.

Main Methods:

Assessed airway Eos recruitment in allergen-challenged WT mice.
Examined Gal-3 expression on Eos cell surface and in secretions.
Performed in vitro flow assays to evaluate Eos rolling, adhesion (VCAM-1, ICAM-1), and migration (eotaxin-1) using WT and Gal-3(-/-) Eos.

Main Results:

Gal-3 expression in lungs correlated with Eos recruitment in allergen-challenged mice.
Gal-3(-/-) Eos showed reduced rolling and stable adhesion, impaired cytoskeletal rearrangement, and lower CD11b expression.
Gal-3(-/-) Eos exhibited significantly decreased migration toward eotaxin-1, suggesting a role for intracellular and/or cell surface Gal-3 in Eos trafficking and migration.

Conclusions:

Lung Gal-3 expression correlates with Eos mobilization in allergic airway inflammation.
Gal-3 on Eos is essential for their trafficking under flow conditions and migration.
Intracellular and/or cell surface Gal-3 signaling is critical for Eos function in allergic airway inflammation.