Premium
Chronic Exposure to Beta‐Blockers Attenuates Inflammation and Mucous Metaplasia in a Murine Asthma Model
Author(s) -
nguyen long phan,
Omoluabi Ozozoma,
Parra Sergio,
Frieske Joanna,
Clement Cecilia,
Ho Samuel,
Knoll Brian J,
Tuvim Michael J,
Dickey Burton F,
Bond Richard A
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.918.3
Subject(s) - metaplasia , medicine , bronchoalveolar lavage , inflammation , immunology , mucin , goblet cell , eosinophil , squamous metaplasia , pathology , asthma , cytokine , epithelium , lung
Based upon analogies to recent changes in the treatment of heart failure, we previously showed that chronic administration of certain ‘beta‐blockers’ decreased airway hyperresponsiveness (AHR) in a murine model of allergic asthma. To elucidate the mechanism for the beneficial effects, we used the same murine model to examine the effects of chronic administration of beta‐blockers on inflammation and mucous metaplasia, cardinal features of asthma that may contribute to AHR. Chronic administration of beta‐blockers reduced the total cell counts and eosinophils in bronchoalveolar lavage (BAL) of antigen‐challenged and sensitized mice. There was also reduced mucin production and goblet cell formation (mucous metaplasia) as determined by periodic acid Schiff's staining. A similar effect was observed by a second laboratory using a different strain of mice (C57BL/6J instead of BALB/cJ), with ~ 90% reduction in eosinophils and mucous metaplasia. These results were confirmed by a decrease in Muc5AC staining of airway epithelium using immunohistochemistry and Muc5AC transcript levels. BAL cytokine levels of IL‐13, IL‐10, IL‐5, and TGF‐â1 were also decreased. These observations suggest that asthmatics may benefit from treatment with beta‐blockers given their ability to reduce various indices of airway inflammation including mucous metaplasia, and inflammatory cells and cytokines in BAL.