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Microbiology 155 (2009), 3500-3508; DOI  10.1099/mic.0.031443-0
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Microbiology 155 (2009), 3500-3508; DOI  10.1099/mic.0.031443-0
© 2009 Society for General Microbiology

Pseudomonas aeruginosa recognizes and responds aggressively to the presence of polymorphonuclear leukocytes

Morten Alhede1,2, Thomas Bjarnsholt2,3, Peter Ø. Jensen3, Richard Kerry Phipps1, Claus Moser3, Lars Christophersen3, Louise Dahl Christensen2, Maria van Gennip2, Matt Parsek4, Niels Høiby3, Thomas Bovbjerg Rasmussen5 and Michael Givskov2

1 Department of Systems Biology, Technical University of Denmark, DK-2800 Lyngby, Denmark
2 Department of International Health, Immunology and Microbiology, University of Copenhagen, DK-2200 Copenhagen, Denmark
3 Department of Clinical Microbiology, Rigshospitalet, DK-2100 Copenhagen Ø, Denmark
4 University of Washington School of Medicine Seattle, Seattle, WA 98195-7242, USA
5 Department of Physiology, Chr. Hansen A/S, DK-2970 Hørsholm, Denmark

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.

Correspondence
Michael Givskov
mgivskov{at}sund.ku.dk

Abbreviations: AHL, N-acylhomoserine lactone; BAL, broncheoalveolar lavage; CF, cystic fibrosis; C4-HSL, N-butanoyl-L-homoserine lactone; 3-oxo-C12-HSL, N-3-oxododecanoyl-L-homoserine lactone; DAPI, 4',6-diamidino-2-phenylindole; LDH, lactate dehydrogenase; PI, propidium iodide; PMN, polymorphonuclear leukocyte; PNA FISH, peptide nucleic acid fluorescence in situ hybridization; PQS, Pseudomonas quinolone signal; QS, quorum sensing

The microarray data discussed in this publication have been deposited in NCBI's Gene Expression Omnibus (GEO, http://www.ncbi.nlm.nih.gov/geo/) and are accessible through GEO Series accession number GSE6769.

Two supplementary tables are available with the online version of this paper.




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Shielding, a new pathogen defence mechanism against PMNs
Microbiology, November 1, 2009; 155(11): 3474 - 3475.
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