Systemic and mucosal pre-administration of recombinant Helicobacter pylori neutrophil-activating protein prevents ovalbumin-induced allergic asthma in mice.

Abstract

Previous epidemiologic studies have demonstrated an inverse association between Helicobacter pylori infection and the frequency of allergic asthma. The neutrophil-activating protein (NAP) of H. pylori has been identified as a modulator possessing anti-Th2 inflammation activity. Here, we sought to determine whether systemic or mucosal pre-administration of recombinant H. pylori NAP (rNAP) could prevent ovalbumin (OVA)-induced allergic asthma in mice. Mice were exposed to purified rNAP through intraperitoneal injection or inhalation and then sensitized with OVA. Following a challenge with aerosolized OVA, the bronchoalveolar lavage fluid (BALF) cell count, lung tissue histology, BALF cytokines and serum IgE were evaluated. Both intraperitoneal injection and inhalation of rNAP prior to OVA sensitization significantly reduced eosinophil accumulation and inflammatory infiltration in lung tissue in OVA-induced asthma mice; eosinophils were reduced in the BALF of rNAP-treated mice. In addition, IL-4 and IL-13 levels were lower (P < 0.01), IL-10 and IFN-γ levels were higher (P < 0.01) and IgE serum levels were lower (P < 0.01) in the treated groups compared to the control group. Systemic and mucosal pre-administration of rNAP could suppress the development of OVA-induced asthma in mice; rNAP may be utilized as part of novel strategies for the prevention or treatment of allergic diseases.