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.