Beneficial Effect of Anti-Interleukin-33 on the Murine Model of Allergic Inflammation of the Lower Airway

Abstract

Objective. Interleukin (IL)-33, which mediates the T_h2 allergic pathway, may play a key role in allergic airway inflammation. This study was conducted to evaluate the therapeutic potential of anti-IL-33 antibody for treatment of allergic inflammation of the lower airway in a murine model. Methods. Twenty-four BALB/c mice were used in this study. Saline was used for sensitization and challenge of mice in Group A (control group, n = 6). Mice in Group B (ovalbumin (OVA) group, n = 6) received intraperitoneal (ip) and intranasal OVA challenge. In Group C (control IgG group, n = 6), mice received ip injection with control IgG prior to OVA challenge. Mice in Group D (anti-IL-33 group, n = 6) received an ip injection of anti-IL-33 prior to challenge. Measurements of serum total and OVA-specific IgE and the number of eosinophils, neutrophils, and lymphocytes in bronchoalveolar lavage (BAL) fluid were performed. We performed histopathologic examination to evaluate the degree of eosinophilic infiltration in lung tissue. Airway hyperreactivity was measured according to change of enhanced pause (Penh). Results. A significant decrease in serum total and OVA-specific IgE and the number of eosinophils and neutrophils in BAL fluid was observed in Group D, compared with Group B or Group C (p < .05). In Group D, treatment with anti-IL-33 resulted in a significant decrease in eosinophilic infiltration in lung tissue, compared with Group B and Group C (p < .05). Degree of airway hyperreactivity, measured by Penh, showed a significant decrease in the anti-IL-33 treatment group, compared with the OVA group or the control IgG treatment group (p < .01, at 50 mg/mL of methacholine). Conclusions: Anti-IL-33 has therapeutic potential for treatment of allergic inflammation of the lower airway.

• airway
• allergy
• anti-IL-33
• bronchoalveolar lavage
• murine
• ovalbumin

Acknowledgments

Young Hyo Kim has received support from an INHA University Research Grant. Chang-Shin Park has received grant support from INHA University and was also supported by research fund (E00004) from National Research Foundation of Korea. Dae Hyun Lim has received grant support from INHA University Hospital Environmental Health Center and Ministry of Environment, Republic of Korea. Sung-Hye Ahn has no relationships to declare. Byong Kwan Son and Jeong Hee Kim have received grant support from INHA University Hospital Environmental Health Center and Ministry of Environment, Republic of Korea. Tae Young Jang has received grant support from INHA University.

Declaration of Interest

The authors report no conflicts of interest. The authors alone are responsible for the content and writing of this article.