Interleukin 5 deficiency abolishes eosinophilia, airways hyperreactivity, and lung damage in a mouse asthma model.
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TLDR
Results indicate that IL-5 and eosinophils are central mediators in the pathogenesis of allergic lung disease.Abstract:
Airways inflammation is thought to play a central role in the pathogenesis of asthma. However, the precise role that individual inflammatory cells and mediators play in the development of airways hyperreactivity and the morphological changes of the lung during allergic pulmonary inflammation is unknown. In this investigation we have used a mouse model of allergic pulmonary inflammation and interleukin (IL) 5-deficient mice to establish the essential role of this cytokine and eosinophils in the initiation of aeroallergen-induced lung damage and the development of airways hyperreactivity. Sensitization and aerosol challenge of mice with ovalbumin results in airways eosinophilia and extensive lung damage analogous to that seen in asthma. Aeroallergen-challenged mice also display airways hyperreactivity to beta-methacholine. In IL-5-deficient mice, the eosinophilia, lung damage, and airways hyperreactivity normally resulting from aeroallergen challenge were abolished. Reconstitution of IL-5 production with recombinant vaccinia viruses engineered to express this factor completely restored aeroallergen-induced eosinophilia and airways dysfunction. These results indicate that IL-5 and eosinophils are central mediators in the pathogenesis of allergic lung disease.read more
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The role of interleukin-5 (IL-5) in vivo: studies with IL-5 deficient mice.
TL;DR: Although the IL-5 deficient mice cannot elicit a pronounced eosinophilia in response to inflammatory stimulation following aeroallergen challenge or parasite infection they still produce basal levels of eOSinophils that appear to be morphologically and functionally normal, however, the basal Levels of eos inophils appear insufficient for normal host defense as IL- 5 deficiency has now been shown to compromise defense against several helminth infections.
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A potent dimeric peptide antagonist of interleukin-5 that binds two interleukin-5 receptor α chains
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Recombinant human interleukin 5 is a selective activator of human eosinophil function.
Angel F. Lopez,Colin J. Sanderson,Jennifer R. Gamble,Hugh Campbell,Ian G. Young,Mathew A. Vadas +5 more
TL;DR: Human rIL-5 was found to selectively stimulate morphological changes and the function of human eosinophils, and is thus a prime candidate for the selective eOSinophilia and eos inophil activation seen in disease.