4034 Th2 Dominant Airway Inflammation Induced By House Dust Mite Chitin Is Dependent on TNF-a and NKT Cell.

Saturday, 17 October 2015
Hall D1 Foyer (Floor 3) (Coex Convention Center)

Da-Il Yoon, MD , Ewha Womans University Mokdong Hospital, Seoul, South Korea

Jun-Pyo Choi, PhD , Ewha Institute of Convergence Medicine, Ewha Womans University Medical Center, Seoul, South Korea

Han-Byul Choi, MD , Ewha Womans University Mokdong Hospital, Seoul, South Korea

Hyeon-Il Choi, PhD , Ewha Institute of Convergence Medicine, Ewha Womans University Medical Center, Seoul, South Korea

Yoon-Keun Kim, MD, PhD , Ewha Institute of Convergence Medicine, Ewha Womans University Medical Center, Seoul, South Korea

Th2 dominant airway inflammation induced by house dust mite chitin is dependent on TNF-a and NKT cell.

 

Background: Chitin is polymer of N-acetyl-b-D-glucosamin and founded in various organism such as house dust mite. Generally, chitin is applied in medical material, because it is known to not induce the immune response. However, according to recent reports, chitin induced innate & adaptive immune response. In this point, we can postulate that HDM chitin induce the immune response, but exact effect & mechanism is unknown.

Objective: To evaluate the immunological side in the development of airway inflammation induced by sensitization with allergens plus house dust mite derived chitin.

 

Method: To induce the airway inflammation by HDM derived chitin, 6 weeks-old mice were administrated intranasally four times with 75 μg of ovalbomin (OVA) and 100 μg of HDM chitin, and then challenged intranasally 4 times with 50 μg of OVA on days 14, 15, 21, and 22. Lung inflammation and immunologic parameters were evaluated 48 h after the final allergen challenge and 6 h after allergen challenge on day 21, respectively.

Result: Intranasal administration of HDM (house dust mite) induced Th2 dominant, but mixed, airway inflammation and chitinase treatment induced down-regulation of Th2 immune response. Refined HDM chitin with allergen sensitization up-regulated the production of Th2 cytokine, dominantly, and chitinase treatment showed similar manner of HDM treatment results. This immune responses are mediated through TLR2, which is known to receptor of chitin recognition, and macrophage derived TNF-a and NKT cell.

Conclusion: These findings indicate that airway inflammation sensitized by HDM derived chitin induces Th2 dominant immune response, which is mainly dependent on TNF-a produced by macrophage cell and NKT cell.