Mucosal exposure to cockroach extract induces allergic sensitization and allergic airway inflammation

• Published in: Allergy, asthma, and clinical immunology asthma, and clinical immunology, 2011-12, Vol.7 (1), p.22-22, Article 22
• Main Authors: Arizmendi, Narcy G, Abel, Melanie, Puttagunta, Lakshmi, Asaduzzaman, Muhammad, Davidson, Courtney, Karimi, Khalil, Forsythe, Paul, Vliagoftis, Harissios
• Format: Article
• Language: English
• Subjects: Analysis; Asthma; Care and treatment; Cockroaches; Health aspects; Immunoglobulin G
• ISSN: 1710-1492; 1710-1484; 1710-1492
• DOI: 10.1186/1710-1492-7-22

Allergic sensitization to aeroallergens develops in response to mucosal exposure to these allergens. Allergic sensitization may lead to the development of asthma, which is characterized by chronic airway inflammation. The objective of this study is to describe in detail a model of mucosal exposure to cockroach allergens in the absence of an exogenous adjuvant. Cockroach extract (CE) was administered to mice intranasally (i.n.) daily for 5 days, and 5 days later mice were challenged with CE for 4 consecutive days. A second group received CE i.n. for 3 weeks. Airway hyperresponsiveness (AHR) was assessed 24 h after the last allergen exposure. Allergic airway inflammation was assessed by BAL and lung histology 48 h after the last allergen exposure. Antigen-specific antibodies were assessed in serum. Lungs were excised from mice from measurement of cytokines and chemokines in whole lung lysate. Mucosal exposure of Balb/c mice to cockroach extract induced airway eosinophilic inflammation, AHR and cockroach-specific IgG1; however, AHR to methacholine was absent in the long term group. Lung histology showed patchy, multicentric damage with inflammatory infiltrates at the airways in both groups. Lungs from mice from the short term group showed increased IL-4, CCL11, CXCL1 and CCL2 protein levels. IL4 and CXCL1 were also increased in the BAL of cockroach-sensitized mice in the short-term protocol. Mucosal exposure to cockroach extract in the absence of adjuvant induces allergic airway sensitization characterized by AHR, the presence of Th2 cytokines in the lung and eosinophils in the airways.