Published ahead of print on April 19, 2007, doi:10.1164/rccm.200608-1243OC Am. J. Respir. Crit. Care Med., Volume 176, Number 1, July 2007, 27-35 A more recent version of this article appeared on July 1, 2007
Submitted on August 31, 2006 Galectin-9 Inhibits CD44-hyaluronan Interaction and Suppresses a Murine Model of Allergic AsthmaShigeki Katoh1*,1 Department of Cell Regulation, Faculty of Medicine, Kagawa University, Kagawa, Japan, 2 Research Division, GalPharma Co Ltd, Takamatsu, Japan, 3 Department of Immunology and Immunopathology, Faculty of Medicine, Kagawa University, Kagawa, Japan, 4 Department of Endocrinology, Faculty of Medicine, Kagawa University, Kagawa, Japan, 5 Division of Human Health and Medical Science, Graduate School of Kuroshio Science, Kochi University, Nankoku, Japan * To whom correspondence should be addressed. E-mail: kshigeki{at}med.kagawa-u.ac.jp.
Rationale: Galectin-9 (Gal-9) belongs to the galectin family that exhibits affinity for Key words: allergy, airway hyper-responsiveness, experimental model, galectin-9 ligand
This article has been cited by other articles:
|
|
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
-galactosides. Gal-9 has a variety of biological activities; however its role in allergic inflammation is unknown.
Objectives: We evaluated the effect of a stable form of the human protein on allergic airway inflammation in a mite allergen-induced asthma model.
Methods: Human stable gal-9 was given by intravenous injection to mice during antigen challenge. The effect of gal-9 on airway inflammation and airway hyper-responsiveness (AHR) was then evaluated.
Measurements and Main Results: Gal-9 reduced AHR as well as T helper type 2 (Th2)-associated airway inflammation. Furthermore, administration of gal-9 as well as anti-CD44mAb inhibited the infiltration of peripheral blood Th2 cells into the airway. Interestingly, gal-9 directly bound the CD44 adhesion molecule and inhibited interactions with hyaluronan (HA). Consistent with the concept that CD44-HA interactions mediate the migration of T cells into the lung, gal-9 blocked CD44-dependent adhesion of BW5147 mouse T cells to HA.
Conclusions: We conclude that gal-9 inhibits allergic inflammation of the airway and AHR by modulating CD44 dependent leukocyte recognition of the extracellular matrix.
