Experimental Model of Pulmonary Allergic Inflammation Induced by Latex in Balb/c

• Main Authors: Parvaneh Farzaneh, Zuhair Mohammad Hassan, Zahra Pourpak, Ahmad Zavaran Hoseini, Ahmad Reza Baghestani, Simon Hogan
• Format: Article
• Language: English
• Published: Royan Institute (ACECR), Tehran 2005-01-01
• Series: Cell Journal
• Subjects: Eosinophilic allergic airway inflammation; Latex; Model; Mouse
• Online Access: http://celljournal.org/library/upload/article/92-97.ps.pdf

Introduction: The prevalence of allergic airway diseases has dramatically increased in recent years all over the world. Murine models of allergic airway inflammation have provided helpful information about treatment and cellular and molecular mechanisms of the disease. Previous published works using murine models to investigate latex allergy did not introduce a complete characteristic eosinophilic allergic airway inflammation. Latex allergy is important due to serious health impacts and widespread use of its products. Thus, the aim of this study was to establish a new mouse model of latex allergic airway inflammation using aerosol inhalation. Materials and Methods: Initially, four groups of mice were injected intraperitoneally (IP) with 0, 10, 50, or 200 µg of latex extract and their serum anti-latex IgE titers were compared using ELISA to find out the optimum dose for IP injection. In the second stage, a standard protocol of inhalation was designed and three doses of latex extract solutions including 1%, 0.1%, and 0.01% were used to induce allergic airway inflammation. Characteristics of this model were shown by studying different parameters including bronchoalveolar lavage (BAL), cytokines (Interleukin-5 [IL-5] and interleukin-13 [IL-13]) and serum anti-latex IgE and IgG1 titers by ELISA, specific histologic changes in the lung and eosinophilia of the bone marrow, peripheral blood, BAL, and lung inflammatory foci. Results: The aerosol inhalation of 1% latex allergens solution and pre-sensitization with 50 µg of latex in this study resulted in the development of characteristic allergic airway inflammation in BALB/c mice. These features included elevated allergen specific IgE and IgG1, peripheral blood, BAL and bone marrow eosinophilia and characteristic inflammatory response in lung with eosinophil infiltration. Elevated levels of IL-5 and IL-13 can be a sign of this type of inflammation. Conclusion: This paper describes a latex aerosol inhalational challenge model of eosinophilic airway inflammation in latex pre-sensitized BALB/c mice.