期刊
NATURE MEDICINE
卷 8, 期 9, 页码 1018-1023出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/nm748
关键词
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资金
- NHLBI NIH HHS [P50-HL56383, K08-HL03788, HL-36110] Funding Source: Medline
- NIDCR NIH HHS [P01-DE13499] Funding Source: Medline
- NIDDK NIH HHS [DK-50305] Funding Source: Medline
- NIGMS NIH HHS [GM-38765] Funding Source: Medline
The prevalence of asthma continues to increase and its optimal treatment remains a challenge. Here, we investigated the actions of lipoxin A(4) (LXA(4)) and its leukocyte receptor in pulmonary inflammation using a murine model of asthma. Allergen challenge initiated airway biosynthesis of LXA(4) and increased expression of its receptor. Administration of a stable analog of LXA(4) blocked both airway hyper-responsiveness and pulmonary inflammation, as shown by decreased leukocytes and mediators, including interleukin-5, interleukin-13, eotaxin, prostanoids and cysteinyl leukotrienes. Moreover, transgenic expression of human LXA(4) receptors in murine leukocytes led to significant inhibition of pulmonary inflammation and eicosanoid-initiated eosinophil tissue infiltration. Inhibition of airway hyper-responsiveness and allergic airway inflammation with a stable LXA(4) analog highlights a unique counter-regulatory profile for the LXA(4) system and its leukocyte receptor in airway responses. Moreover, our findings suggest that lipoxin and related pathways offer novel multi-pronged therapeutic approaches for human asthma.
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