Galectin-9 in allergic airway inflammation and hyper-responsiveness in mice

Erna Sziksz, G. Kozma, E. Pállinger, Zsolt István Komlósi, C. Ádori, Lajos Kovács, B. Szebeni, K. Rusai, G. Losonczy, András Szabó, A. Vannay

Research output: Contribution to journalArticle

21 Citations (Scopus)

Abstract

Background: Galectin-9 (Gal-9) is a member of the growing family of β-galactoside-binding lectins. Gal-9 is an eosinophil chemoattractant and inducer of Th1 cell apoptosis. These effects suggest its potential role in the pathogenesis of asthma. Our aim was to study the expression of Gal-9 in an ovalbumin (OVA)-induced mouse model of allergic asthma. Methods: To investigate the significance of Gal-9 in allergic inflammation and airway hyperresponsiveness (AHR), a group of BALB/c mice was sensitized and challenged with OVA (GOVA). Another group of animals was allergized with OVA and also treated with dexamethasone (DEX) (GOVA+DEX). The control group (GPBS) received phosphate-buffered saline instead of OVA as placebo. Airway reactivity to intravenous methacholine was assessed. Results: The percentage of Gal-9-positive cells and their intracellular Gal-9 content and Th1/Th2 cytokine levels in the bronchoalveolar lavage (BAL) were determined by flow cytometry. Gal-9 mRNA expression and protein level were measured in the lung tissue by real-time RT-PCR and Western blot. In GOVAmice, airway inflammation and mucus hypersecretion developed. DEX treatment inhibited the main features of experimental asthma. The number of Gal-9-positive lymphocytes, eosinophil and neutrophil granulocytes and the levels of Th2 cytokines were higher in the BAL of GOVA compared to GPBS or G OVA+DEXmice. Moreover, Gal-9 protein level was elevated in the lungs of GOVA mice. Conclusions: These results suggest that Gal-9 plays a role as a mediator contributing to the development of allergic airway inflammation. Gal-9 may serve as a recruiter of eosinophil granulocytes and promoter of Th2 dominance.

Original languageEnglish
Pages (from-to)308-317
Number of pages10
JournalInternational Archives of Allergy and Immunology
Volume151
Issue number4
DOIs
Publication statusPublished - Mar 2010

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Respiratory Hypersensitivity
Galectins
Inflammation
Ovalbumin
Eosinophils
Dexamethasone
Asthma
Bronchoalveolar Lavage
Granulocytes
Cytokines
Galactosides
Lung
Th1 Cells
Methacholine Chloride
Chemotactic Factors
Mucus
Helper-Inducer T-Lymphocytes
Lectins

Keywords

  • Allergic inflammation
  • Animal model
  • Asthma
  • Eosinophils
  • Galectin-9

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

Cite this

Galectin-9 in allergic airway inflammation and hyper-responsiveness in mice. / Sziksz, Erna; Kozma, G.; Pállinger, E.; Komlósi, Zsolt István; Ádori, C.; Kovács, Lajos; Szebeni, B.; Rusai, K.; Losonczy, G.; Szabó, András; Vannay, A.

In: International Archives of Allergy and Immunology, Vol. 151, No. 4, 03.2010, p. 308-317.

Research output: Contribution to journalArticle

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abstract = "Background: Galectin-9 (Gal-9) is a member of the growing family of β-galactoside-binding lectins. Gal-9 is an eosinophil chemoattractant and inducer of Th1 cell apoptosis. These effects suggest its potential role in the pathogenesis of asthma. Our aim was to study the expression of Gal-9 in an ovalbumin (OVA)-induced mouse model of allergic asthma. Methods: To investigate the significance of Gal-9 in allergic inflammation and airway hyperresponsiveness (AHR), a group of BALB/c mice was sensitized and challenged with OVA (GOVA). Another group of animals was allergized with OVA and also treated with dexamethasone (DEX) (GOVA+DEX). The control group (GPBS) received phosphate-buffered saline instead of OVA as placebo. Airway reactivity to intravenous methacholine was assessed. Results: The percentage of Gal-9-positive cells and their intracellular Gal-9 content and Th1/Th2 cytokine levels in the bronchoalveolar lavage (BAL) were determined by flow cytometry. Gal-9 mRNA expression and protein level were measured in the lung tissue by real-time RT-PCR and Western blot. In GOVAmice, airway inflammation and mucus hypersecretion developed. DEX treatment inhibited the main features of experimental asthma. The number of Gal-9-positive lymphocytes, eosinophil and neutrophil granulocytes and the levels of Th2 cytokines were higher in the BAL of GOVA compared to GPBS or G OVA+DEXmice. Moreover, Gal-9 protein level was elevated in the lungs of GOVA mice. Conclusions: These results suggest that Gal-9 plays a role as a mediator contributing to the development of allergic airway inflammation. Gal-9 may serve as a recruiter of eosinophil granulocytes and promoter of Th2 dominance.",
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AU - Sziksz, Erna

AU - Kozma, G.

AU - Pállinger, E.

AU - Komlósi, Zsolt István

AU - Ádori, C.

AU - Kovács, Lajos

AU - Szebeni, B.

AU - Rusai, K.

AU - Losonczy, G.

AU - Szabó, András

AU - Vannay, A.

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