TY - JOUR
T1 - Pseudomonas aeruginosa recognizes and responds aggressively to the presence of polymorphonuclear leukocytes
AU - Alhede, Morten
AU - Bjarnsholt, T.
AU - Jensen, P.O.
AU - Phipps, Richard Kerry
AU - Moser, C.
AU - Christophersen, L.
AU - Christensen, L.D.
AU - van Gennip, M.
AU - Parsek, M.
AU - Hoiby, N.
AU - Rasmussen, T.B.
AU - Givskov, M.
PY - 2009
Y1 - 2009
N2 - 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 (OS) 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.
AB - 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 (OS) 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.
U2 - 10.1099/mic.0.031443-0
DO - 10.1099/mic.0.031443-0
M3 - Journal article
C2 - 19643762
SN - 1350-0872
VL - 155
SP - 3500
EP - 3508
JO - Microbiology (United Kingdom)
JF - Microbiology (United Kingdom)
IS - Part 11
ER -