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Mice lacking the VIP gene show airway hyperresponsiveness and airway inflammation, partially reversible by VIP.

Authors: Szema, AM  Hamidi, SA  Lyubsky, S  Dickman, KG  Mathew, S  Abdel-Razek, T  Chen, JJ  Waschek, JA  Said, SI 
Citation: Szema AM, etal., Am J Physiol Lung Cell Mol Physiol. 2006 Nov;291(5):L880-6. Epub 2006 Jun 16.
Pubmed: (View Article at PubMed) PMID:16782752
DOI: Full-text: DOI:10.1152/ajplung.00499.2005

The mechanisms leading to asthma, and those guarding against it, are yet to be fully defined. The neuropeptide VIP is a cotransmitter, together with nitric oxide (NO), of airway relaxation, and a modulator of immune and inflammatory responses. NO-storing molecules in the lung were recently shown to modulate airway reactivity and were proposed to have a protective role against the disease. We report here that mice with targeted deletion of the VIP gene spontaneously exhibit airway hyperresponsiveness to the cholinergic agonist methacholine as well as peribronchiolar and perivascular cellular infiltrates and increased levels of inflammatory cytokines in bronchoalveolar lavage fluid. Immunologic sensitization and challenge with ovalbumin generally enhanced the airway hyperresponsiveness and airway inflammation in all mice. Intraperitoneal administration of VIP over a 2-wk period in knockout mice virtually eliminated the airway hyperresponsiveness and reduced the airway inflammation in previously sensitized and challenged mice. The findings suggest that 1) VIP may be an important component of endogenous anti-asthma mechanisms, 2) deficiency of the VIP gene may predispose to asthma pathogenesis, and 3) treatment with VIP or a suitable agonist may offer potentially effective replacement therapy for this disease.

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CRRD Object Information
CRRD ID: 5685620
Created: 2012-01-12
Species: All species
Last Modified: 2012-01-12
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.