4.3 Article

Severe Vitamin E deficiency modulates airway allergic inflammatory responses in the murine asthma model

Journal

FREE RADICAL RESEARCH
Volume 42, Issue 4, Pages 387-396

Publisher

TAYLOR & FRANCIS LTD
DOI: 10.1080/10715760801976600

Keywords

eosinophils; allergic inflammation; asthma; cytokines; IgE; vitamin E

Funding

  1. NHLBI NIH HHS [K08-HL76415, K08 HL076415, K08 HL076415-02] Funding Source: Medline
  2. NIEHS NIH HHS [R01 ES011985-01A2, R01 ES011985-02, R01 ES011985-03, R01 ES011985, ES011985] Funding Source: Medline
  3. NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [K08HL076415] Funding Source: NIH RePORTER
  4. NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES [R01ES011985] Funding Source: NIH RePORTER

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Allergic asthma is a complex immunologically mediated disease associated with increased oxidative stress and altered antioxidant defenses. It was hypothesized that alpha-tocopherol (alpha-T) decreases oxidative stress and therefore its absence may influence allergic inflammatory process, a pathobiology known to be accompanied by oxidative stress. Therefore, selected parameters of allergic asthma sensitization and inflammation were evaluated following ovalbumin sensitization and rechallenge of alpha-T transfer protein (TTP) knock-out mice (TTP-/-) that have greatly reduced lung alpha-T levels (e.g. <5%) compared to their litter mate controls (TTP+/+). Results showed that severe alpha-T deficiency result in a blunted lung expression of IL-5 mRNA and IL-5 protein and plasma IgE levels compared with TTP+/+ mice following immune sensitization and rechallenge, although lung lavage eosinophil levels were comparable in both genomic strains. It is concluded that the initial stimulation of immune responses by the TTP-/- mice were generally blunted compared to the TTP+/+ mice, thus diminishing some aspects of subsequent allergic inflammatory processes.

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