Pseudomonas aeruginosa recognizes and responds aggressively to the presence of polymorphonuclear leukocytes.
Polymorphonuclear neutrophilic leukocytes (PMNs) play a central role in innate immunity, where they dominate the response to infections, in particular in the cystic fibrosis lung. PMNs are phagocytic cells that produce a wide range of antimicrobial agents aimed at killing invading bacteria. However, the opportunistic pathogen Pseudomonas aeruginosa can evade destruction by PMNs and thus cause persistent infections. In this study, we show that biofilm cells of P. aeruginosa recognize the presence of attracted PMNs and direct this information to their fellow bacteria through the quorum sensing (QS) signalling system. The bacteria respond to the presence of PMNs by upregulating synthesis of a number of QS-controlled virulence determinants including rhamnolipids, all of which are able to cripple and eliminate cells of the host defence. Our in vitro and in vivo analyses support a 'launch a shield' model by which rhamnolipids surround the biofilm bacteria and on contact eliminate incoming PMNs. Our data strengthen the view that cross-kingdom communication plays a key role in P. aeruginosa recognition and evasion of the host defence.
Alhede
Morten
M
Department of International Health, Immunology and Microbiology, University of Copenhagen, DK-2200 Copenhagen, Denmark.|Department of Systems Biology, Technical University of Denmark, DK-2800 Lyngby, Denmark.
Bjarnsholt
Thomas
T
Department of Clinical Microbiology, Rigshospitalet, DK-2100 Copenhagen Ø, Denmark.|Department of International Health, Immunology and Microbiology, University of Copenhagen, DK-2200 Copenhagen, Denmark.
Jensen
Peter Ø
PØ
Department of Clinical Microbiology, Rigshospitalet, DK-2100 Copenhagen Ø, Denmark.
Phipps
Richard Kerry
RK
Department of Systems Biology, Technical University of Denmark, DK-2800 Lyngby, Denmark.
Moser
Claus
C
Department of Clinical Microbiology, Rigshospitalet, DK-2100 Copenhagen Ø, Denmark.
Christophersen
Lars
L
Department of Clinical Microbiology, Rigshospitalet, DK-2100 Copenhagen Ø, Denmark.
Christensen
Louise Dahl
LD
Department of International Health, Immunology and Microbiology, University of Copenhagen, DK-2200 Copenhagen, Denmark.
van Gennip
Maria
M
Department of International Health, Immunology and Microbiology, University of Copenhagen, DK-2200 Copenhagen, Denmark.
Parsek
Matt
M
University of Washington School of Medicine Seattle, Seattle, WA 98195-7242, USA.
Høiby
Niels
N
Department of Clinical Microbiology, Rigshospitalet, DK-2100 Copenhagen Ø, Denmark.
Rasmussen
Thomas Bovbjerg
TB
Department of Physiology, Chr. Hansen A/S, DK-2970 Hørsholm, Denmark.
Givskov
Michael
M
Department of International Health, Immunology and Microbiology, University of Copenhagen, DK-2200 Copenhagen, Denmark.
D000818:Animals; D018441:Biofilms / Q000254:growth & development*; D001992:Bronchoalveolar Lavage Fluid / Q000382:microbiology; D004269:DNA, Bacterial / Q000235:genetics; D004399:Dynorphins / Q000494:pharmacology; D005260:Female; D015964:Gene Expression Regulation, Bacterial; D006017:Glycolipids / Q000378:metabolism; D008171:Lung Diseases / Q000276:immunology / Q000382:microbiology; D051379:Mice; D008807:Mice, Inbred BALB C; D009504:Neutrophils / Q000276:immunology*; D020411:Oligonucleotide Array Sequence Analysis; D011552:Pseudomonas Infections / Q000276:immunology / Q000382:microbiology*; D011550:Pseudomonas aeruginosa / Q000235:genetics / Q000276:immunology* / Q000472:pathogenicity; D053038:Quorum Sensing; D014774:Virulence
D004269:DNA, Bacterial; D006017:Glycolipids; C418382:rhamnolipid; D004399:Dynorphins