Pseudomonas aeruginosa eradicates Staphylococcus aureus by manipulating the host immunity
Erwan Pernet,
Laurent Guillemot,
Pierre-Régis Burgel,
Clémence Martin,
Gérard Lambeau,
Isabelle Sermet-Gaudelus,
Dorota Sands,
Dominique Leduc,
Philippe C. Morand,
Louise Jeammet,
Michel Chignard,
Yongzheng Wu () and
Lhousseine Touqui ()
Additional contact information
Erwan Pernet: Unité de défense innée et inflammation, Institut Pasteur
Laurent Guillemot: Unité de défense innée et inflammation, Institut Pasteur
Pierre-Régis Burgel: Université Paris Descartes, Sorbonne Paris Cité
Clémence Martin: Université Paris Descartes, Sorbonne Paris Cité
Gérard Lambeau: Institut de Pharmacologie Moléculaire et Cellulaire, UMR 7275 Centre National de la Recherche Scientifique et Université de Nice Sophia Antipolis
Isabelle Sermet-Gaudelus: INSERM U 806, Université René Descartes, CRCM, Service de Pneumo-Pédiatrie, Hôpital Necker-Enfants Malades
Dorota Sands: Institute of Mother and Child, CF Centre
Dominique Leduc: Unité de défense innée et inflammation, Institut Pasteur
Philippe C. Morand: Université Paris Descartes, Sorbonne Paris Cité
Louise Jeammet: Institut de Pharmacologie Moléculaire et Cellulaire, UMR 7275 Centre National de la Recherche Scientifique et Université de Nice Sophia Antipolis
Michel Chignard: Unité de défense innée et inflammation, Institut Pasteur
Yongzheng Wu: Unité de défense innée et inflammation, Institut Pasteur
Lhousseine Touqui: Unité de défense innée et inflammation, Institut Pasteur
Nature Communications, 2014, vol. 5, issue 1, 1-11
Abstract:
Abstract Young cystic fibrosis (CF) patients’ airways are mainly colonized by Staphylococcus aureus, while Pseudomonas aeruginosa predominates in adults. However, the mechanisms behind this infection switch are unclear. Here, we show that levels of type-IIA-secreted phospholipase A2 (sPLA2-IIA, a host enzyme with bactericidal activity) increase in expectorations of CF patients in an age-dependent manner. These levels are sufficient to kill S. aureus, with marginal effects on P. aeruginosa strains. P. aeruginosa laboratory strains and isolates from CF patients induce sPLA2-IIA expression in bronchial epithelial cells from CF patients (these cells are a major source of the enzyme). In an animal model of lung infection, P. aeruginosa induces sPLA2-IIA production that favours S. aureus killing. We suggest that sPLA2-IIA induction by P. aeruginosa contributes to S. aureus eradication in CF airways. Our results indicate that a bacterium can eradicate another bacterium by manipulating the host immunity.
Date: 2014
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Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:5:y:2014:i:1:d:10.1038_ncomms6105
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DOI: 10.1038/ncomms6105
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