Wednesday, 14 October 2015
Hall D1 Foyer (Floor 3) (Coex Convention Center)
Jin-Young Lee, MD, PhD
,
Health Promotion Center, Samsung Medical Center, Seoul, South Korea
Young Hee Lim, MD, PhD
,
Ansan Sarang General Hospital, Ansan, South Korea
Mi-Jung Oh, MD, PhD
,
Bundang Jaesang Hospital, Bundang, South Korea
Kyoung Won Ha, MD
,
Seoul Samsung Medical Clinic, Incheon, South Korea
Jae-Won Paeng
,
Samsung Biomedical Research Institute, Seoul, South Korea
Sehyo Yune, MD
,
Department of Medicine, Samsung Medical Center, Seoul, South Korea
Byung-Jae Lee, MD, PhD
,
Samsung Medical Center, Seoul, South Korea
Dong-Chull Choi, MD, PhD
,
Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, South Korea
Jin-Young Lee, MD, PhD
,
Health Promotion Center, Samsung Medical Center, Seoul, South Korea
Purpose: The expression of nitric oxide synthase-2 (NOS-2) and levels of exhaled nitric oxide (NO) are increased in allergic airway diseases. However, whether the upregulation of NOS has a deleterious effect on airway inflammation and hyperresponsiveness remains controversial. We aimed to clarify the pathophysiological role of NOS-2 in competition with arginase, using NOS-2 knockout mice in models of allergic asthma.
Methods: We compared airway inflammation and hyperresponsiveness, as well as arginase expression, using NOS or arginase inhibitors in 6-week-old female C57BL/6, and NOS-2 knockout mice.
Results: Airway hyperresponsiveness was unaffected by NOS-2 depeletion or NOS inhibition. However, airway inflammation was aggravated in NOS-2 knockout mice than in wild-type mice with augmentation of arginase I expression. Inhibition of arginase attenuated airway inflammation in wild-type and NOS-2 knockout mice.
Conclusions: NOS-2 knockout mice showed increased ovalbumin-induced airway inflammation with augmentation of arginase I expression. Our results suggested that imbalance between NOS-2 and arginase with augmentation of arginase I expression resulted in aggravation of airway inflammation, and inhibitors of arginase I may be effective in suppressing allergic inflammation
