Bacterial quorum sensing molecule induces chemotaxis of human neutrophils via induction of p38 and leukocyte specific protein 1 (LSP1)

When bacteria colonize surfaces, they socialize and form biofilms. This process is well regulated and relies on the communication among the bacteria via so-called “quorum sensing molecules”. Among those, N-(3-oxododecanoyl)-l-homoserine lactone (AHL-12), generated by Pseudomonas aeruginosa and other...

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Hauptverfasser: Kahle, Nadine (VerfasserIn) , Hänsch, Gertrud Maria (VerfasserIn)
Dokumenttyp: Article (Journal)
Sprache:Englisch
Veröffentlicht: 2013
In: Immunobiology
Year: 2012, Jahrgang: 218, Heft: 2, Pages: 145-151
ISSN:1878-3279
DOI:10.1016/j.imbio.2012.02.004
Online-Zugang:Verlag, Volltext: http://www.sciencedirect.com/science/article/pii/S017129851200040X
Verlag, Volltext: http://dx.doi.org/10.1016/j.imbio.2012.02.004
Volltext
Verfasserangaben:N.A. Kahle, G. Brenner-Weiss, J. Overhage, U. Obst, G.M. Hänsch

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520 |a When bacteria colonize surfaces, they socialize and form biofilms. This process is well regulated and relies on the communication among the bacteria via so-called “quorum sensing molecules”. Among those, N-(3-oxododecanoyl)-l-homoserine lactone (AHL-12), generated by Pseudomonas aeruginosa and other Gram-negative bacteria, activates not only bacteria but also interacts with mammalian cells. Among others, it activates phagocytic cells and - as we had shown previously - it is chemotactic for human polymorphonuclear neutrophils (PMN) in vitro. In the present study, we analyzed the signalling pathway of AHL-12 in PMN. We focused on the mitogen activated protein (MAP) kinase p38, because SB203580, an inhibitor of p38, prevented the AHL-12 induced chemotaxis. We found that in response to AHL-12, p38 was phosphorylated within minutes, as was its downstream target, the MAPKAP-Kinase-2 (MK2). In PMN, the major substrate of MK2 is the leukocyte specific protein 1 (LSP1), which binds to F-actin and participates directly in actin polymerization and cell migration. In response to AHL-12, LSP1 was phosphorylated and co-localized with F-actin in polarized PMN, suggesting that AHL-12-induced migration depended on p38 and LSP1 activation. 
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