<i>Staphylococcus aureus</i> Adenosine Inhibits sPLA2-IIA–Mediated Host Killing in the Airways

DOI PDF 被引用文献2件
  • Erwan Pernet
    Unité de Défense Innée et Inflammation/INSERM U874, Institut Pasteur , 75015 Paris ,
  • Jérémy Brunet
    Unité de Défense Innée et Inflammation/INSERM U874, Institut Pasteur , 75015 Paris ,
  • Laurent Guillemot
    Unité de Défense Innée et Inflammation/INSERM U874, Institut Pasteur , 75015 Paris ,
  • Michel Chignard
    Unité de Défense Innée et Inflammation/INSERM U874, Institut Pasteur , 75015 Paris ,
  • Lhousseine Touqui
    Unité de Défense Innée et Inflammation/INSERM U874, Institut Pasteur , 75015 Paris ,
  • Yongzheng Wu
    Unité de Défense Innée et Inflammation/INSERM U874, Institut Pasteur , 75015 Paris ,

書誌事項

公開日
2015-06-01
権利情報
  • https://academic.oup.com/pages/standard-publication-reuse-rights
DOI
  • 10.4049/jimmunol.1402665
公開者
Oxford University Press (OUP)

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<jats:title>Abstract</jats:title> <jats:p>Staphylococcus aureus is a common cause of bacterial infections in respiratory diseases. It secretes molecules to dampen host immunity, and the recently identified adenosine is one of these molecules. The type IIA secretory phospholipase A2 (sPLA2-IIA) is a host protein endowed with antibacterial properties, especially against Gram-positive bacteria such as S. aureus. However, the role of adenosine in sPLA2-IIA–mediated S. aureus killing by host is still unknown. The present studies showed that the S. aureus mutant lacking adenosine production (∆adsA strain) increased sPLA2-IIA expression in guinea pig airways and was cleared more efficiently, compared with the wild-type strain. S. aureus ∆adsA strain induced sPLA2-IIA expression by alveolar macrophages after phagocytic process via NOD2–NF-κB–dependent mechanism. However, S. aureus adenosine (wild-type and adsA-complemented strains) and exogenous adenosine downregulated S. aureus phagocytosis by alveolar macrophages, leading to inhibition of sPLA2-IIA expression. This occurred through inhibition of p38 phosphorylation via adenosine receptors A2a-, A2b-, and protein kinase A–dependent pathways. Taken together, our studies suggest that, in the airway, S. aureus escapes sPLA2-IIA–mediated killing through adenosine-mediated inhibition of phagocytosis and sPLA2-IIA expression.</jats:p>

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