2056 Dexamethasone Can Reverse the Alteration of Airway Epithelial Responses to Rhinovirus Infection by Th2 Cytokines

Monday, 5 December 2011
Poster Hall (Cancún Center)

Min-Suk Yang, MD , Department of Internal Medicine, Seoul National University College of Medicine, Seoul, South Korea

Hyun-Seung Lee, PhD , Department of Internal Medicine, Seoul National University College of Medicine, Seoul, South Korea

Woo-Jung Song , Department of Internal Medicine, Seoul National University College of Medicine, Seoul, South Korea

So-Hee Lee , Department of Internal Medicine, Seoul National University College of Medicine, Seoul, South Korea

Heung-Woo Park , Department of Internal Medicine, Seoul National University College of Medicine, Seoul, South Korea

Sang-Heon Cho , Department of Internal Medicine, Seoul National University College of Medicine, Seoul, South Korea

Kyung-Up Min , Department of Internal Medicine, Seoul National University College of Medicine, Seoul, South Korea

Yoon-Seok Chang, MD, PhD , Department of Internal Medicine, Seoul National University Bundang Hospital, Seongnam, South Korea

Background: Human rhinovirus (HRV) triggers exacerbation of asthma by induction of diverse pro-inflammatory mediators. However, the effect of Th2 cytokine milieu on the HRV infection is not clearly evaluated although several investigations suggested have defective expression of type I interferon (IFN) in asthmatics. The aim of this study was to examine altered expression of anti-viral type I IFN against HRV by Th2 cytokines (IL-4 or IL-13) and therapeutic effect of dexamethasone.

Methods: Human rhinovirus 1B (HRV1B)-infected BEAS-2B cells were stimulated with IL-4 or IL-13. Dexamethasone or medium were preincubated for 30 min before the stimulation with Th2 cytokines. mRNA expression of IFN-β, CC chemokines, CXCL chemokines, and pro-inflammatory cytokines was measured by Real time PCR with SYBR Green.

Results: HRV1B infection in Th2 cytokines milieu showed significant reduction of IFN-β expression. In contrast, HRV1B infection with Th2 cytokines enhanced the induction of eotaxin-1, RANTES and IL-6 expression. Dexamethasone restored the suppressed IFN-β expression and decreased eotaxin-1 and IL-6 mRNA expression by Th2 cytokines in HRV1B infected BEAS-2B cell.

Conclusions: Th2 cytokine milieu diminishes IFN-β expression and enhances eotaxin-1, RANTES and IL-6 expression in HRV infected in bronchial epithelial cell and these alterations can be reversed by dexamethasone.