Clinical & Experimental Allergy

Lyprinol reduces inflammation and improves lung function in a mouse model of allergic airways disease

Authors

  • L. G. Wood,

    1. Centre for Asthma and Respiratory Diseases and Hunter Medical Research Institute, The University of Newcastle, Newcastle, NSW, Australia
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    • *These authors contributed equally to this manuscript

  • L. C. Hazlewood,

    1. Centre for Asthma and Respiratory Diseases and Hunter Medical Research Institute, The University of Newcastle, Newcastle, NSW, Australia
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    • *These authors contributed equally to this manuscript

  • P. S. Foster,

    1. Centre for Asthma and Respiratory Diseases and Hunter Medical Research Institute, The University of Newcastle, Newcastle, NSW, Australia
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  • P. M. Hansbro

    1. Centre for Asthma and Respiratory Diseases and Hunter Medical Research Institute, The University of Newcastle, Newcastle, NSW, Australia
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Correspondence:
A/Prof Philip M. Hansbro, Centre for Asthma and Respiratory Diseases, The University of Newcastle, Level 5, David Maddison Clinical Sciences Building, Newcastle, NSW, Australia. E-mail: Philip.Hansbro@newcastle.edu.au

Summary

Background Asthma is an inflammatory airway disease that is characterized by an influx of eosinophils to the lungs, mucus hypersecretion and T helper type 2 cytokine production. Recent dietary changes, including a decreased ω-3 polyunsaturated fatty acid (PUFA) intake, may have contributed to increased asthma rates and dietary supplementation with marine oil could have clinical benefits.

Objective To assess the effects of dietary supplementation with ω-3 PUFAs on allergic inflammation and lung function using a mouse model of ovalbumin (OVA)-induced allergic airway disease (AAD).

Methods BALB/c mice received a daily supplement of either fish oil (rich in ω-3 PUFA) or lyprinol (a complex mixture of various marine lipids plus vitamin E and olive oil) before and during AAD. The effects of supplementation on AAD were assessed.

Results Lyprinol but not fish oil treatment reduced eosinophil influx into the bronchoalveolar lavage fluid, the lung tissue surrounding the airways and the blood, decreased mucus hypersecretion in the lung and reduced airway hyperresponsiveness (AHR). The effects of lyprinol were not associated with changes in serum IgG1 or IgG2a, or the release of IL-4, IL-5, IL-13 and IFN-γ.

Conclusions Lyprinol suppresses the development of allergic inflammation and AHR in AAD. The therapeutic potential of dietary supplementation with lyprinol for asthma warrants further investigation.

Cite this as: L. G. Wood, L. C. Hazlewood, P. S. Foster and P. M. Hansbro, Clinical & Experimental Allergy, 2010 (40) 1785–1793.

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