%0 Journal Article %A Alhede, Morten %A Bjarnsholt, Thomas %A Jensen, Peter Ø. %A Phipps, Richard Kerry %A Moser, Claus %A Christophersen, Lars %A Christensen, Louise Dahl %A van Gennip, Maria %A Parsek, Matt %A Høiby, Niels %A Rasmussen, Thomas Bovbjerg %A Givskov, Michael %T Pseudomonas aeruginosa recognizes and responds aggressively to the presence of polymorphonuclear leukocytes %D 2009 %J Microbiology, %V 155 %N 11 %P 3500-3508 %@ 1465-2080 %R https://doi.org/10.1099/mic.0.031443-0 %K 3-oxo-C12-HSL, N-3-oxododecanoyl-l-homoserine lactone %K CF, cystic fibrosis %K DAPI, 4′,6-diamidino-2-phenylindole %K PQS, Pseudomonas quinolone signal %K PNA FISH, peptide nucleic acid fluorescence in situ hybridization %K QS, quorum sensing %K LDH, lactate dehydrogenase %K PMN, polymorphonuclear leukocyte %K BAL, broncheoalveolar lavage %K PI, propidium iodide %K C4-HSL, N-butanoyl-l-homoserine lactone %K AHL, N-acylhomoserine lactone %I Microbiology Society, %X 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. %U https://www.microbiologyresearch.org/content/journal/micro/10.1099/mic.0.031443-0