Wednesday, 14 October 2015
Hall D1 Foyer (Floor 3) (Coex Convention Center)
Hyun Ji Song
,
Soonchunhyang University, Asan, South Korea
Taehyeong Lee
,
Division of Allergy and Respiratory Medicine, Soonchunhyang University Bucheon Hospital, Bucheon, South Korea
Ji Ah Jun
,
Division of Allergy and Respiratory Medicine, Soonchunhyang University Bucheon Hospital, Bucheon, South Korea
Hun Soo Chang, PhD
,
Division of Allergy and Respiratory Medicine, Soonchunhyang University Bucheon Hospital, Bucheon, South Korea
Jong-Sook Park, MD
,
Division of Allergy and Respiratory Medicine, Soonchunhyang University Bucheon Hospital, Bucheon, South Korea
Choon-Sik Park, MD., PhD.
,
Soonchunhyang University Bucheon Hospital, Asan, South Korea
Backgrounds: We previously reported elevation of S100A9 protein in sputum of neutrophilic severe uncontrolled asthmatics compared with stable asthmatics [Annals of allergy, asthma, immunology on 2013 Oct;111(4):268-275] suggesting possible role of S100A9 in neutrophilic severe asthma. IL-1beta(IL-1β) and IL-18, which are released by activated inflammasome, exert neutrophil - activating activities. The aim of this study was to evaluate the temporal relationship of S100A9 with inflammasome activation in neutrophilicmurine C57BL/6 mice model using CFA/OVA-sensitization/challenge.
Methods: Expression of S100A9, S100A8 mRNA and protein levels and activated caspase-1 were measured in the lung tissues of the CFA/OVA modelusing a RT-PCR, real-time PCR and western blot. Spatial expression of S100A9 protein and inflammasome - related proteins were visualized by immune fluorescent stain. To evaluate the relation of S100A9 on activation of inflammsome, temporal changes of neutrophil infiltration and activation of caspase-1 were analyzed after intra-tracheal administration of 10ug S100A9 protein.
Results: S100A9 and P20 - activated caspase-1 started to increase from day 14 and peaked at day 23,earlier than the number of total cells, macrophage and neutrophils significantly increased with concomitant increase of airway resistance at day 23. Neutrophil elastase, S100A9 and activated caspase-1 co-localized on peri-bronchially infiltrating cells and apical portion of bronchial epitheliumusing confocal microscopy. Intra-tracheal instillation of S100A9 protein induced rapid increase of activated caspase-1 in the lung tissue from 2 hr, peaked at 8 hr, then progressively decreased till 80 hr with concomitantincrease of neutrophilsin BAL fluids
Conclusions: S100A9 may induces neutrophilic inflammation via direct activation of inflammsome in the airway.
