Abstract | BACKGROUND: METHODS: RESULTS: Although the caveolin-1 deficient mice had greater lung inflammatory indices compared to wild-type mice, they exhibited reduced AHR following LPS exposure. The uncoupling of inflammation and AHR led us to investigate the role of caveolin-1 in the production of nitric oxide, which is known to act as a bronchodilator. The absence of caveolin-1 resulted in increased nitrite levels in the lavage fluid in both sham and LPS treated mice. Additionally, inducible nitric oxide synthase expression was increased in the lung tissue of caveolin-1 deficient mice following LPS exposure and administration of the potent and specific inhibitor 1400W increased AHR to levels comparable to wild-type mice. CONCLUSIONS: We attribute the relative airway hyporesponsiveness in the caveolin-1 deficient mice after LPS exposure to the specific role of caveolin-1 in mediating nitric oxide production.
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Authors | Bethany J Hsia, Amy M Pastva, Charles D Giamberardino, Erin N Potts-Kant, W Michael Foster, Loretta G Que, Soman N Abraham, Jo Rae Wright, David W Zaas |
Journal | Journal of allergy & therapy
(J Allergy Ther)
Vol. Suppl 1
Issue 4
(Jan 25 2012)
ISSN: 2155-6121 [Print] United States |
PMID | 24273688
(Publication Type: Journal Article)
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