- Title
- Dietary lycopene supplementation suppresses Th2 responses and lung eosinophilia in a mouse model of allergic asthma
- Creator
- Hazlewood, Leia C.; Wood, Lisa G.; Hansbro, Philip M.; Foster, Paul S.
- Relation
- Journal of Nutritional Biochemistry Vol. 22, Issue 1, p. 95-100
- Publisher Link
- http://dx.doi.org/10.1016/j.jnutbio.2009.12.003
- Publisher
- Elsevier
- Resource Type
- journal article
- Date
- 2011
- Description
- Allergic airways disease (AAD) is associated with an increased influx of eosinophils to the lungs, mucus hypersecretion and Th2 cytokine production. Dietary antioxidant supplementation may alter cytokine responses and thus allergic inflammation. Lycopene is a potent dietary antioxidant. The objective of this study was to investigate the effects of lycopene, on allergic inflammation, in a mouse model of AAD. BALB/c mice receiving lycopene supplement or control were intraperitoneally sensitised and intranasally challenged with ovalbumin (OVA) to induce AAD. The effect of supplementation on inflammatory cell influx into bronchoalveolar lavage fluid, lung tissue and blood, mucus-secreting cell numbers in the airways, draining lymph node OVA-specific cytokine release, serum IgG1 levels and lung function in AAD was assessed. Supplementation reduced eosinophilic infiltrates in the bronchoalveolar lavage fluid, lung tissue and blood, and mucus-secreting cell numbers in the airways. The OVA-specific release of Th2-associated cytokines IL-4 and IL-5 was also reduced. We conclude that supplementation with lycopene reduces allergic inflammation both in the lungs and systemically, by decreasing Th2 cytokine responses. Thus, lycopene supplementation may have a protective effect against asthma.
- Subject
- lycopene; antioxidants; asthma; airway inflammation; eosinophils; Th2 response
- Identifier
- http://hdl.handle.net/1959.13/936494
- Identifier
- uon:12329
- Identifier
- ISSN:0955-2863
- Language
- eng
- Reviewed
- Hits: 3417
- Visitors: 3375
- Downloads: 0
Thumbnail | File | Description | Size | Format |
---|