Chitin and β-Glucan Polysaccharides as Immunomodulators of Airway Inflammation and Atopic Disease
Adriana Catalli and Marianna Kulka
Affiliation: National Research Council Canada, 550 University Avenue, Room 432, Charlottetown, PE, C1A 4P3, Canada.
Polysaccharides are receiving increased attention due to their clinical applications in tissue engineering, vaccine development, nutritional supplementation and antimicrobial biopolymer engineering. The most abundant polysaccharides include fungal cell wall components chitin and β-1,3-glucans. Recent evidence has shown that these polysaccharides modulate airway inflammation, making them the basis of several drug discovery platforms. Small to intermediate chitin fragments ( < 70 μm) are protective in allergic inflammatory models, skewing T cell immunity towards Th1 responses, and reducing the production of Th2 cytokines. As such, chitin prevents the development of the quintessential features of asthmatic disease including chronic airway inflammation, airway hyperresponsiveness and pathological remodeling changes in mouse models of allergy. In contrast, the in vivo effects of β-glucans in animal models of airway inflammation are often contradictory, and the number of human studies is limited. β-1,3-glucans are both proand anti-inflammatory, preventing and enhancing allergic inflammation depending on the preparation, purity and species origin of the β-glucans. This review summarizes recent studies of chitin and β-glucans in models of atopy and airway inflammation and examines the possible reasons for the apparently contradictory observations. Recent relevant patents are also highlighted.
Keywords: Chitin, β-glucan, allergy, asthma, inflammation, airway, Dectin-1, TLR2, glucan, hyperresponsiveness, bronchodilators, glycoproteins, mannans, -1,4 linked N-acetyl-D-gluco-samine, uridine diphosphate-N-acetylglucosamine, Chitin synthase enzymes, pattern recognition receptors, pathogen-associated molecular patterns, mannose receptor, CD206, immunoreceptor tyro-sine-based activation, ITAM, NFAT, ERK MAPK, CARD9, MALT1, IKK, MyD88, TIRAP/Mal, TRAF6, TAK1, Aspergillus fumigatus, bacillus Calmette-Guerin, Mycobacterium bovis, ovalbumin, Dermatophagoides pteronyssinus, Sclerotinia sclerotiorum, Penecillium chrysogenum, Clados-porium herbarum, Grifolan
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