Fat-1 transgenic mice with elevated omega-3 fatty acids are protected from allergic airway responses.
Fat-1 transgenic mice with elevated omega-3 fatty acids are protected from allergic airway responses.
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DOI:
10.1016/j.bbadis.2011.05.002
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发表时间:
2011-09
影响因子:
6.2
通讯作者:
Kang, Jing X.
中科院分区:
文献类型:
--
作者:
Bilal, Sueleyman;Haworth, Oliver;Wu, Lijun;Weylandt, Karsten H.;Levy, Bruce D.;Kang, Jing X.
Omega-3 polyunsaturated fatty acids (n-3 PUFA) have been implicated in the alleviation of asthma. Recent studies have demonstrated that the n-3 PUFA derived lipid mediators, protectin D1 and resolvin E1, may act as potent resolution agonists in airway inflammation. The effects of the n-3 PUFA tissue status itself on asthma pathogenesis remains to be further investigated. In this study allergic airway inflammation induced by allergen sensitization and aerosol challenge in Fat-1 and wild-type (WT) mice was investigated. Fat-1 transgenic mice displayed increased endogenous lung n-3 PUFA. When allergen-sensitized and aerosol-challenged, these animals had decreased airway inflammation with decreased leukocyte accumulation in bronchoalveolar lavage fluid (BALF) and lung parenchyma. The Fat-1 mice had a shift to the right in the dose-response relationship for methacholine induced bronchoconstriction with a significant increase in the log ED200. The Fat-1 mice had lower BALF concentrations of the pro-inflammatory cytokines IL-1α, IL-2, IL-5, IL-9, IL- 13, G-CSF, KC and RANTES. Furthermore, increased lung tissue amounts of the counter-regulatory mediators protectin D1 and resolvin E1 were found in Fat-1 mice after bronchoprovocative challenge. These results therefore demonstrate a direct protective role for lung n-3 PUFA in allergic airway responses and an increased generation of protectin D1 and resolvin E1 in this context.
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影响因子:
2.8
作者:
Yokoyama, A;Hamazaki, T;Hiwada, K
通讯作者:
Hiwada, K
影响因子:
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Simopoulos, A. P.
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Simopoulos, A. P.
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30.5
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Haworth, Oliver;Cernadas, Manuela;Levy, Bruce D.
通讯作者:
Levy, Bruce D.
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作者:
Kang JX;Wang J
通讯作者:
Wang J
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24.3
作者:
SCHWARTZ, J;WEISS, ST
通讯作者:
WEISS, ST