Petasites extract Ze 339 (PET) inhibits allergen-induced Th2 responses, airway inflammation and airway hyperreactivity in mice

Background: The herbal Petasites hybridus (butterbur) extract (Ze 339, PET) is known to have leukotriene inhibiting properties, and therefore might inhibit allergic diseases. Methods: The effect of PET was investigated in ovalbumin (OVA) immunized BALB/c mice given intranasally together with antigen...

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Veröffentlicht in:Phytotherapy research 2010-05, Vol.24 (5), p.680-685
Hauptverfasser: Brattström, A., Schapowal, A., Maillet, I., Schnyder, B., Ryffel, B., Moser, R.
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Sprache:eng
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Zusammenfassung:Background: The herbal Petasites hybridus (butterbur) extract (Ze 339, PET) is known to have leukotriene inhibiting properties, and therefore might inhibit allergic diseases. Methods: The effect of PET was investigated in ovalbumin (OVA) immunized BALB/c mice given intranasally together with antigen challenge in the murine model of allergic airway disease (asthma) with the analysis of the inflammatory and immune parameters in the lung. Results: PET given with the antigen challenge inhibited the allergic response. PET inhibited airway hyperresponsiveness (AHR) and eosinophil recruitment into the bronchoalveolar lavage (BAL) fluid upon allergen challenge, but had no effect in the saline control mice. Eosinophil recruitment was further assessed in the lung by eosinophil peroxidase (EPO) activity at a concentration of 100 µg PET. Microscopic investigations revealed less inflammation, eosinophil recruitment and mucus hyperproduction in the lung with 100 µg PET. Diminution of AHR and inflammation was associated with reduced IL‐4, IL‐5 and RANTES production in the BAL fluid with 30 µg PET, while OVA specific IgE and eotaxin serum levels remained unchanged. Conclusion: PET, which has been reported to inhibit leukotriene activity, reduced allergic airway inflammation and AHR by inhibiting the production of the Th2 cytokines IL‐4 and IL‐5, and RANTES. Copyright © 2009 John Wiley & Sons, Ltd.
ISSN:0951-418X
1099-1573
1099-1573
DOI:10.1002/ptr.2972