期刊
FREE RADICAL RESEARCH
卷 42, 期 4, 页码 387-396出版社
TAYLOR & FRANCIS LTD
DOI: 10.1080/10715760801976600
关键词
eosinophils; allergic inflammation; asthma; cytokines; IgE; vitamin E
资金
- NHLBI NIH HHS [K08-HL76415, K08 HL076415, K08 HL076415-02] Funding Source: Medline
- NIEHS NIH HHS [R01 ES011985-01A2, R01 ES011985-02, R01 ES011985-03, R01 ES011985, ES011985] Funding Source: Medline
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [K08HL076415] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES [R01ES011985] Funding Source: NIH RePORTER
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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