Abstract
Chitin, which is a major component of house dust mites (HDM), fungi, crustaceans, etc., can activate immune cells, suggesting that it contributes to development of allergic disorders such as asthma. Although the pathophysiological sensitization route of asthmatic patients to allergens is considered via the respiratory tract, the roles of intranasally-administered chitin in development of asthma remain unclear. After ovalbumin (OVA) challenge, development of airway inflammation was profoundly exacerbated in mice sensitized with OVA in the presence of chitin. The exacerbation was dependent on IL-33, but not IL-25, thymic stromal lymphopoietin or IL-17A. Chitin enhanced IL-33-dependent IL-1β production by dendritic cells (DCs). Furthermore, chitin- and IL-33-stimulated DC-derived IL-1β promoted OVA-specific Th2 cell activation, resulting in aggravation of OVA-induced airway inflammation. These findings indicate the adjuvant activity of chitin via a new mechanism and provide important clues for development of therapeutics for allergic disorders caused by HDM, fungi and crustaceans.
Highlights
Chitin, β-(1-4)-poly-N-acetyl-D-glucosamine, is widely distributed in nature as the second most abundant polysaccharide after cellulose
We found that the proportion and number of IL-13+ Th2 cells were significantly increased in both the lungs and bronchoalveolar lavage fluids (BALFs) from mice sensitized with OVA in the presence of chitin compared with the other groups (Fig. 2b,c)
It was reported that inhalation of chitin alone resulted in induction of airway eosinophilia in mice[11,13], suggesting that chitin may be somehow involved in the pathogenesis of house dust mites (HDM)-mediated asthma
Summary
Β-(1-4)-poly-N-acetyl-D-glucosamine, is widely distributed in nature as the second most abundant polysaccharide after cellulose It is a common structural component in lower organisms: in the cell wall of pathogens such as bacteria and fungi, the sheath of parasitic nematodes, and the exoskeleton of crustaceans (crabs and shrimp) and insects[1,2,3,4,5]. Intraperitoneal administration of ovalbumin (OVA) to mice in the presence of chitin particles enhanced activation of ovalbumin (OVA)-specific Th2 cells as well as Th1 cells and Th17 cells, contributing to development of OVA-induced Th2 cell-mediated airway inflammation[14]. TLR2 and IL-17 are required for the effect of chitin as an adjuvant in the setting It remains unclear how IL-17, which is produced by macrophages through interaction of chitin with TLR2, contributes to Th2 cell-mediated airway eosinophilia. The effect of intranasally–administered chitin on Th2 cell-mediated airway inflammation needs to be elucidated
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