Saturday, 17 October 2015
Hall D1 Foyer (Floor 3) (Coex Convention Center)
Seung-Hwa Lee
,
Asan Institute for Life Sciences, Seoul, South Korea
Seon-Joo Yoon
,
Neopharm Co., Ltd., Seoul, South Korea
Ha-Jung Kim
,
Asan Institute for Life Sciences, Seoul, South Korea
Eun Lee, MD
,
Department of Pediatrics, Childhood Asthma Atopy Center, Environmental Health Center, Asan Medical Center, University of Ulsan College of Medicine, Seoul, South Korea
Song-I Yang, MD
,
Department of Pediatrics, Hallym University Sacred Heart Hospital, Anyang, South Korea
Young-Ho Jung, MD
,
Department of Pediatrics, Bundang CHA Medical Center, CHA University School of Medicine, Seongnam, South Korea
Ho-Sung Yu, Master of Science
,
Asan Institute for Life Science, Asan Medical Center, Seoul, South Korea
Hee-Suk Kim
,
Asan Institute for Life Sciences, Seoul, South Korea
Yeon Hee Park
,
Asan Institute for Life Sciences, Seoul, South Korea
So-Yeon Lee, MD
,
Department of Pediatrics, Hallym Sacred Heart Hospital, Hallym University College of Medicine, Anyang, South Korea
Jun-Sung Park
,
Asan Medical Center, Seoul, South Korea
Hyun Ok Jun
,
Asan Medical Center, Soeul, South Korea
Background: Immunoglobulin E (IgE) triggers multiple inflammatory allergic responses and cytokine release when it binds to high-affinity IgE Fc receptor (FcεRI) on mast cells in atopic dermatitis (AD) and asthma. Anti-FcεRI antibody is a new option for treatment that may block IgE-FcεRI binding and therefore may reduce inflammatory cascade in allergic diseases. However, the potential effects and mechanism of anti-FcεRI antibody remain poorly understood.
Objective: We investigated the effect and mechanisms of anti-FcεRI antibody by blocking the combination of IgE-FcεRI antibody in allergic march (AM) mice model.
Methods: We developed mice model of AM with three 1-week exposures (separated by 2-weeks interval) to an ovalbumin (OVA) or saline followed by OVA inhalation (challenge). In order to develop a mice model of AM, the day before sacrifice, all mice inhaled 1% OVA as the airway challenge. Anti-FcεRI antibody was administered to the mice intraperitoneally for 4 consecutive days before the end of study. Identification of interleukin (IL)-17 expression was performed by immunohistochemistry and real time PCR on skin and lung specimens.
Results: Anti-FcεRI antibody treated AM mice had significantly decreased phenotypes (e.g., clinical score, airway hyperresponsiveness, and pathology) of AD and allergic asthma. In addition, the levels of total IgE, OVA-specific IgG1 and IL-13 in serum were significantly lower in AM mice treated with anti-FcεRI antibody. The level of prostaglandin D2 and the number of mast cells in skin were also decreased in the anti-FcεRI antibody treated with AM mice. Furthermore, the skin and lung expressions of IL-17 were reduced after the treatment of anti-FcεRI antibody.
Conclusion: IgE-FcεRI blockade by Anti-FcεRI antibody can suppress the IgE-mediated phenotypes and inflammatory responses in AM. And its mechanism may be the decrease in IL-17 via the suppression of FcεRI–mediated mast cell activation.
