Development of eosinophilic airway inflammation and airway hyperresponsiveness requires interleutkin-5 but not immunoglobulin E or B lymphocytes
Development of eosinophilic airway inflammation and airway hyperresponsiveness requires interleutkin-5 but not immunoglobulin E or B lymphocytes
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DOI:
10.1165/ajrcmb.21.4.3659
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发表时间:
1999-10-01
影响因子:
6.4
通讯作者:
Gelfand, EW
中科院分区:
文献类型:
--
作者:
Hamelmann, E;Takeda, K;Gelfand, EW
We previously defined a role for B cells and allergen-specific immunoglobulins in the development of allergic sensitization, airway inflammation, and airway hyperresponsiveness (AHR), using a 10-d protocol in which allergen exposure occurred exclusively via the airways, without adjuvant. In the present protocol, normal and B-cell-deficient (mu Mt(-/-)) mice were sensitized intraperitoneally to ovalbumin (OVA) and challenged with OVA via the airways in order to examine the requirements for AHR with this protocol. T-cell activation (antigen-specific proliferative responses and Th2-type cytokine production) and eosinophil infiltration in the peribronchial regions of the airways, with signs of eosinophil activation and degranulation, occurred in both experimental groups. In contrast to the 10-d protocol, increased in vivo airway responsiveness to methacholine and in vitro tracheal smooth-muscle responses to electrical field stimulation were observed in both normal and B-cell-deficient mice, and these responses were inhibited by anti-interleukin (IL)-5 administration before airway challenge. These data show that IL-5, but not B cells or allergen-specific IgE, are required for eosinophil airway infiltration and the development of AHR following allergen/alum sensitization and repeated airway challenge with allergen. These results emphasize that the use of different sensitization and challenge protocols can influence the requirements for development of AHR.