Ginger prevents Th2-mediated immune responses in a mouse model of airway inflammation

It is well documented that compounds from rhizomes of Zingiber officinale, commonly called ginger, have anti-inflammatory properties. Here, we show that ginger can exert such functions in vivo, namely in a mouse model of Th2-mediated pulmonary inflammation. The preparation of ginger aqueous extract...

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Published in:International immunopharmacology Vol. 8; no. 12; pp. 1626 - 1632
Main Authors: Ahui, Marie Louise Berthe, Champy, Pierre, Ramadan, Abdulraouf, Pham Van, Linh, Araujo, Luiza, Brou André, Konan, Diem, Séverine, Damotte, Diane, Kati-Coulibaly, Séraphin, Offoumou, Michel Atté, Dy, Michel, Thieblemont, Nathalie, Herbelin, André
Format: Journal Article
Language:English
Published: Amsterdam Elsevier B.V 10-12-2008
Elsevier
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Summary:It is well documented that compounds from rhizomes of Zingiber officinale, commonly called ginger, have anti-inflammatory properties. Here, we show that ginger can exert such functions in vivo, namely in a mouse model of Th2-mediated pulmonary inflammation. The preparation of ginger aqueous extract (Zo.Aq) was characterized by mass spectrometry as an enriched fraction of n-gingerols. Intraperitoneal injections of this extract before airway challenge of ovalbumin (OVA)-sensitized mice resulted in a marked decrease in the recruitment of eosinophils to the lungs as attested by cell counts in bronchoalveolar lavage (BAL) fluids and histological examination. Resolution of airway inflammation induced by Zo.Aq was accompanied by a suppression of the Th2 cell-driven response to allergen in vivo. Thus, IL-4, IL-5 and eotaxin levels in the lungs as well as specific IgE titres in serum were clearly diminished in ginger-treated mice relative to their controls after allergen sensitization and challenge. Finally, we found that [6]-gingerol, a major constituent of ginger, was sufficient to suppress eosinophilia in our model of inflammation. This is the first evidence that ginger can suppress Th2-mediated immune responses and might thus provide a possible therapeutic application in allergic asthma.
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ISSN:1567-5769
1878-1705
DOI:10.1016/j.intimp.2008.07.009