Fax +41 61 306 12 34 E-Mail karger@karger.ch www.karger.com Original Paper Int Arch Allergy Immunol 2010;151:308–317 DOI: 10.1159/000250439 Galectin-9 in Allergic Airway Inflammation and Hyper-Responsiveness in Mice Erna Sziksz a, b Gergely Tibor Kozma b Éva Pállinger c Zsolt István Komlósi d Csaba Ádori e Lajos Kovács a Beáta Szebeni a, b Krisztina Rusai a, b György Losonczy d András Szabó a Ádám Vannay a, f a First Department of Pediatrics, Semmelweis University, b Research Laboratory of Pediatrics and Nephrology, Hungarian Academy of Sciences, c Research Group for Inflammation Biology and Immunogenomics of Hungarian Academy of Sciences and Semmelweis University, d Department of Pulmonology, Semmelweis University, e Laboratory of Neurochemistry and Experimental Medicine, National Institute of Psychiatry and Neurology, f János Szentágothai Knowledge Center, Semmelweis University, Budapest, Hungary by real-time RT-PCR and Western blot. In G OVA mice, airway inflammation and mucus hypersecretion developed. DEX treatment inhibited the main features of experimental asth- ma. The number of Gal-9-positive lymphocytes, eosinophil and neutrophil granulocytes and the levels of Th2 cytokines were higher in the BAL of G OVA compared to G PBS or G OVA+DEX mice. Moreover, Gal-9 protein level was elevated in the lungs of G OVA 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 recruit- er of eosinophil granulocytes and promoter of Th2 domi- nance. Copyright © 2009 S. Karger AG, Basel Introduction The incidence and prevalence of asthma have substan- tially increased in the developed world over the last two decades. Asthma is a complex inflammatory disease of the lung characterized by airway inflammation, airway Key Words Galectin-9  Asthma  Eosinophils  Allergic inflammation  Animal model Abstract Background: Galectin-9 (Gal-9) is a member of the growing family of -galactoside-binding lectins. Gal-9 is an eosino- phil 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 asth- ma. Methods: To investigate the significance of Gal-9 in al- lergic inflammation and airway hyperresponsiveness (AHR), a group of BALB/c mice was sensitized and challenged with OVA (G OVA ). Another group of animals was allergized with OVA and also treated with dexamethasone (DEX) (G OVA+DEX ). The control group (G PBS ) received phosphate-buffered sa- line instead of OVA as placebo. Airway reactivity to intrave- nous 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 ex- pression and protein level were measured in the lung tissue Received: January 14, 2009 Accepted after revision: June 3, 2009 Published online: October 22, 2009 Correspondence to: Dr. Erna Sziksz First Department of Pediatrics Semmelweis University Bókay János utca 53–54, HU–1083 Budapest (Hungary) Tel. +36 1 210 2930, Fax +36 1 313 8212, E-Mail sziksz@gyer1.sote.hu © 2009 S. Karger AG, Basel 1018–2438/10/1514–0308$26.00/0 Accessible online at: www.karger.com/iaa E.S. and G.T.K. contributed equally to this work.