Different challenge terms determine disease patterns of antigen-induced pulmonary inflammation in E3 rats
Authors: SUN, QINGZHU; YANG, XUDONG; ASIM, M. B. RAZA; JIAO, FANGFANG; HE, XIAOJING; ZHONG, BO; LI, DONGMIN; LU, SHEMIN
Source: Apmis, Volume 119, Numbers 4-5, April/May 2011 , pp. 229-238(10)
Abstract:Sun Q, Yang X, Asim MBR, Jiao F, He X, Zhong B, Li D, Lu S. Different challenge terms determine disease patterns of antigen-induced pulmonary inflammation in E3 rats. APMIS 2011; 119: 229–38.
Antigen induced pulmonary inflammation (AIPI) in rats, a classic animal model for asthma, has greatly contributed to the understanding of the disease pathogenesis, especially for the inflammation process. E3 rats are recently used to induce AIPI model for its susceptibility to pulmonary inflammation, but the features of AIPI with different antigen challenge terms on E3 rats require to be elucidated systemically. The aim of this study was to compare AIPI disease patterns in E3 rats with different challenge terms. E3 rats were immunized and challenged with ovalbumin (OVA) for 1, 4, and 8 weeks. Histological methods were used to determine morphological changes in lungs and cell types in bronchoalveolar lavage fluid. Nitric oxide (NO) concentration was assayed by Griess method. IL-4 and TGF-β expression were detected by real-time PCR. ELISA was used for the determination of serum IgE and OVA-specific IgG1. The results showed that all the sensitized E3 rats had a strong influx of eosinophils into the airway. In 1-week challenge group, the rats showed stronger inflammation, such as elevated levels of NO, delayed type hypersensitivity, IL-4 expression, and inflammatory cell infiltration; while in 8-week challenge group, rats manifested significant tissue destruction, accumulation of collagen and mucus production, and higher levels of antibody production, and TGF-β expression. Hence, the detail characterizations of AIPI model challenged for different terms demonstrated that E3 rats challenged with antigen for 1 week are suitable for studying acute pulmonary inflammation; meanwhile, the model established in the rats challenged for 8 weeks is appropriate for understanding pathogenesis of lung remodelling in chronic inflammation.
Document Type: Research Article
Publication date: April 1, 2011