TGase 2 Induces Allergic Asthma by up-Regulating IgE and Mediators in Cross-Talk of B and Mast Cells Via CD40/CD40L in Mice

Abstract

FEBRUARY 2013 AB44 Abstracts S A T U R D A Y 159 Effect of Cholesterol Depletion On Interleukin-8 Production in Human Respiratory Epithelial Cells Min Jung Kim, MD, Jung Yeon Hong, Kyung Eun Lee, PhD, Hwan Soo Kim, MD, Yoon Ki Han, MD, Hye Mi Jee, MD, Kyung Won Kim, MD, PhD, Myung Hyun Sohn, MD, PhD, Kyu-Earn Kim, MD, PhD; Yonsei University College of Medicine, Seoul, Korea, Yonsei University School of Medicine, Seoul, Korea, CHA University School of Medicine, Seongnam, Korea. RATIONALE: Lipid rafts in epithelial cell membrane plays multifunctions, including components of immune system and important mediators in inflammatory process. But the role of cholesterol, composing lipid rafts, has not been described in the inflammatory response. The aim of this study is to investigate the effect of cholesterol depletion to inflammatory process via expression of interleukin (IL)-8 in airway epithelial cells. METHODS: The human epithelial-like lung carcinoma cell line(A 549) was treated with 0.5% methyl-b-cyclodextrin as a selective cholesterol extractor. IL-8 levels were assessed by enzyme-linked immunosorbent assay (ELISA) and rechecked after cholesterol repletion. Mitogen-activated protein kinase (MAPK) inhibitors were used to find upstream signaling pathway for IL-8 production in cholesterol-depleted cells. RESULTS: IL-8 production in cholesterol-depleted epithelial cells increased in a time-dependent manner. The maximum production of IL-8 recorded at 24 hwas almost 3.5 timesmore than control cells. In addition, it reversed after cholesterol repletion. And IL-8 production decreased followed by pretreatment with extracellular signal-regulated kinase (ERK) inhibitor U0126, but not with JNK inhibitor II or p38 MAPK inhibitor SB202190. CONCLUSIONS: These results suggested that inflammatory responses could be increased in cholesterol-depleted cells, and it was regulated by MAPK signaling system, predominantly by ERK pathway. We concluded that lipid component in airway epithelial cells may play a role in inflammatory process.