Objective: We investigated the role of chitin in the induction of Th1, Th2, and Th17 response, sensitizing and challenging mice intranasally with OVA and chitin in this study. We also evaluated the role of TNF-α and the size of chitin in the development of Th2 immune response induced by chitin, using TNF-α-deficient mice and chitinase-treated chitin, respectively.
Methods: A mouse model was generated via simultaneous intranasal administration of 75 μg of ovalbumin (OVA) and 100 μg of house dust mite (HDM)-derived chitin in the presence or absence of chitinase. The effect of TNF-α on adaptive immune response was also evaluated using TNF-α-deficient mice.
Results: HDM-derived chitin induced airway inflammation and increased the expression of all cytokines of Th1, Th2, and Th17 as well as the serum level of OVA-specific IgE, IgG1, and IgG2a. In the absence of TNF-α or in the presence of chitinase, the expression of Th2 cytokines and the serum level of OVA-specific IgE were alleviated, while the expression of Th1 and Th17 cytokines and the serum level of OVA-specific IgG1 and IgG2a were preserved or more enhanced.
Conclusion: HDM-derived chitin is size-dependent multifaceted immune adjuvant inducing Th1, Th2, and Th17 immune response, and TNF-α produced by airway exposure to HDM-derived chitin is a key mediator in the development of Th2 cell response to inhaled allergens.