Allergen-induced airway remodeling is impaired in galectin-3 - Deficient mice

Xiao Na Ge, Nooshin S. Bahaie, Bit Na Kang, M. Reza Hosseinkhani, Sung Gil Ha, Elizabeth M. Frenzel, Fu-Tong Liu, Savita P. Rao, P. Sriramarao

Research output: Contribution to journalArticle

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Abstract

The role played by the β-galactoside - binding lectin galectin-3 (Gal-3) in airway remodeling, a characteristic feature of asthma that leads to airway dysfunction and poor clinical outcome in humans, was investigated in a murine model of chronic allergic airway inflammation. Wild-type (WT) and Gal-3 knockout (KO) mice were subjected to repetitive allergen challenge with OVA up to 12 wk, and bronchoalveolar lavage fluid (BALF) and lung tissue collected after the last challenge were evaluated for cellular features associated with airway remodeling. Compared to WT mice, chronic OVA challenge in Gal-3 KO mice resulted in diminished remodeling of the airways with significantly reduced mucus secretion, subepithelial fibrosis, smooth muscle thickness, and peribronchial angiogenesis. The higher degree of airway remodeling in WT mice was associated with higher Gal-3 expression in the BALF as well as lung tissue. Cell counts in BALF and lung immunohistology demonstrated that eosinophil infiltration in OVA-challenged Gal-3 KO mice was significantly reduced compared with that WT mice. Evaluation of cellular mediators associated with eosinophil recruitment and airway remodeling revealed that levels of eotaxin-1, IL-5, IL-13, found in inflammatory zone 1, and TGF-β were substantially lower in Gal-3 KO mice. Finally, leukocytes from Gal-3 KO mice demonstrated decreased trafficking (rolling) on vascular endothelial adhesion molecules compared with that of WT cells. Overall, these studies demonstrate that Gal-3 is an important lectin that promotes airway remodeling via airway recruitment of inflammatory cells, specifically eosinophils, and the development of a Th2 phenotype as well as increased expression of eosinophil-specific chemokines and profibrogenic and angiogenic mediators.

Original languageEnglish (US)
Pages (from-to)1205-1214
Number of pages10
JournalJournal of Immunology
Volume185
Issue number2
DOIs
StatePublished - Jul 15 2010

Fingerprint

Galectin 3
Airway Remodeling
Allergens
Knockout Mice
Eosinophils
Bronchoalveolar Lavage Fluid
Lectins
Lung
Chemokine CCL11
Galactosides
Interleukin-13
Interleukin-5
Mucus
Chemokines
Smooth Muscle
Blood Vessels
Leukocytes
Fibrosis
Asthma
Cell Count

ASJC Scopus subject areas

  • Immunology
  • Medicine(all)

Cite this

Ge, X. N., Bahaie, N. S., Kang, B. N., Hosseinkhani, M. R., Ha, S. G., Frenzel, E. M., ... Sriramarao, P. (2010). Allergen-induced airway remodeling is impaired in galectin-3 - Deficient mice. Journal of Immunology, 185(2), 1205-1214. https://doi.org/10.4049/jimmunol.1000039

Allergen-induced airway remodeling is impaired in galectin-3 - Deficient mice. / Ge, Xiao Na; Bahaie, Nooshin S.; Kang, Bit Na; Hosseinkhani, M. Reza; Ha, Sung Gil; Frenzel, Elizabeth M.; Liu, Fu-Tong; Rao, Savita P.; Sriramarao, P.

In: Journal of Immunology, Vol. 185, No. 2, 15.07.2010, p. 1205-1214.

Research output: Contribution to journalArticle

Ge, XN, Bahaie, NS, Kang, BN, Hosseinkhani, MR, Ha, SG, Frenzel, EM, Liu, F-T, Rao, SP & Sriramarao, P 2010, 'Allergen-induced airway remodeling is impaired in galectin-3 - Deficient mice', Journal of Immunology, vol. 185, no. 2, pp. 1205-1214. https://doi.org/10.4049/jimmunol.1000039
Ge XN, Bahaie NS, Kang BN, Hosseinkhani MR, Ha SG, Frenzel EM et al. Allergen-induced airway remodeling is impaired in galectin-3 - Deficient mice. Journal of Immunology. 2010 Jul 15;185(2):1205-1214. https://doi.org/10.4049/jimmunol.1000039
Ge, Xiao Na ; Bahaie, Nooshin S. ; Kang, Bit Na ; Hosseinkhani, M. Reza ; Ha, Sung Gil ; Frenzel, Elizabeth M. ; Liu, Fu-Tong ; Rao, Savita P. ; Sriramarao, P. / Allergen-induced airway remodeling is impaired in galectin-3 - Deficient mice. In: Journal of Immunology. 2010 ; Vol. 185, No. 2. pp. 1205-1214.
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