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. 2002 Sep;8(9):1018-23.
doi: 10.1038/nm748. Epub 2002 Aug 12.

Multi-pronged inhibition of airway hyper-responsiveness and inflammation by lipoxin A(4)

Bruce D Levy  1 , George T De Sanctis, Pallavi R Devchand, Eugene Kim, Kate Ackerman, Birgitta A Schmidt, Wojciech Szczeklik, Jeffrey M Drazen, Charles N Serhan
Affiliations

Multi-pronged inhibition of airway hyper-responsiveness and inflammation by lipoxin A(4)

Bruce D Levy et al. Nat Med. 2002 Sep.

Abstract

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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Comment in

  • 'Good' lipids for asthma.
    Peters-Golden M. Peters-Golden M. Nat Med. 2002 Sep;8(9):931-2. doi: 10.1038/nm0902-931. Nat Med. 2002. PMID: 12205450 No abstract available.

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