Erna Sziksz1, Ádám Vannay1 , Éva Pállinger2, Zsolt Komlósi3, Edit Buzás2, András Szabó1, Tivadar Tulassay1, Gergely T Kozma1
11st Department of Pediatrics, Semmelweis University and Research Group for Paediatrics and Nephrology, Hungarian Academy of Scineces, Hungary; 2 Department of Genetics, Cell and Immunobiology, 3Department of Pulmonology, Semmelweis University, Hungary;

The aim of the study: Asthma is a chronic disease of airways, which manifests in childhood. In the pathogenesis of asthma both the innate and adaptive immune responses take part. Sugar dependent mechanisms can influence the immune system but there are only few data coming from asthma research. Galectins are members of lectin family so they bind sugars with high affinity. In our study we investigated the role of galectin-9 (Gal-9) in the pathogenesis of asthma.

Methods: Groups of femaleBALB/c mice were sensitized by i.p. injection of 20 µg ovalbumin (OVA) emulsified in aluminum hydroxide on days 1 and 14. Mice were challenged via the airways with 1% OVA on days 28-30 using nebulization. Control mice were sensitized and challenged with PBS. On day 31 bronchoalveolar lavage (BAL) and lung tissues were obtained for further analysis. The level of Gal-9 mRNA and protein in lungs were determined by real-time PCR and Western blot. Intracellular Gal-9 content and Gal-9 binding capacity of bronchoalveolar cells were measured by flow cytometric (FACS) analysis.

Results: The sensitization and challenge lead to the elevation of Gal-9 level in the lung tissue. According to the FACS analysis the percentage/number of Gal-9 positive alveolar macrophages decreases, but the level of Gal-9 in this cells was significantly increased after OVA challenge. At the same time the OVA sensitization elevated the percentage/number of Gal-9 positive lymphocytes and the Gal-9 binding ability of these cells, but decreased the level of Gal-9 inside the cells.

Conclusion: The present study demonstrates that Gal-9 as eosinophil chemoattractant could have important roles in the pathogenesis of asthma in an animal model.