| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
* Cardiovascular Research Unit, Division of Clinical Sciences (North), and Academic Units of
Infectious Diseases and
Respiratory Medicine, Division of Genomic Medicine, University of Sheffield, Sheffield, United Kingdom;
Laboratory of Microbial Interactions, Department of Molecular and Cellular Interactions, Flanders Interuniversity Institute of Biotechnology, Vrije Universiteit Brussels, Brussels, Belgium; and
¶
Department of Molecular Biology, Massachusetts General Hospital, Wellman 10, Boston, MA 02114
Clearance of neutrophils from inflamed sites is critical for resolution of inflammation, but pathogen-driven neutrophil apoptosis can impair host defenses. We previously showed that pyocyanin, a phenazine toxic metabolite produced by Pseudomonas aeruginosa, accelerates neutrophil apoptosis in vitro. We compared wild-type and pyocyanin-deficient strains of P. aeruginosa in a murine model of acute pneumonia. Intratracheal instillation of either strain of P. aeruginosa caused a rapid increase in bronchoalveolar lavage neutrophil counts up to 18 h after infection. In wild-type infection, neutrophil numbers then declined steadily, whereas neutrophil numbers increased up to 48 h in mice infected with pyocyanin-deficient P. aeruginosa. In keeping with these differences, pyocyanin production was associated with reduced bacterial clearance from the lungs. Neutrophil apoptosis was increased in mice infected with wild-type compared with the phenazine-deficient strain or two further strains that lack pyocyanin production, but produce other phenazines. Concentrations of potent neutrophil chemokines (MIP-2, KC) and cytokines (IL-6, IL-1
) were significantly lower in wild-type compared with phenazine-deficient strain-infected mice at 18 h. We conclude that pyocyanin production by P. aeruginosa suppresses the acute inflammatory response by pathogen-driven acceleration of neutrophil apoptosis and by reducing local inflammation, and that this is advantageous for bacterial survival.
Related articles in The JI:
This article has been cited by other articles:
|
|
 |
|
  H. Liang, L. Li, Z. Dong, M. G. Surette, and K. Duan The YebC Family Protein PA0964 Negatively Regulates the Pseudomonas aeruginosa Quinolone Signal System and Pyocyanin Production J. Bacteriol., September 15, 2008; 190(18): 6217 - 6227. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 I. Nagaoka, F. Niyonsaba, Y. Tsutsumi-Ishii, H. Tamura, and M. Hirata Evaluation of the effect of human {beta}-defensins on neutrophil apoptosis Int. Immunol., April 1, 2008; 20(4): 543 - 553. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 L. R. Prince, S. M. Bianchi, K. M. Vaughan, M. A. Bewley, H. M. Marriott, S. R. Walmsley, G. W. Taylor, D. J. Buttle, I. Sabroe, D. H. Dockrell, et al. Subversion of a Lysosomal Pathway Regulating Neutrophil Apoptosis by a Major Bacterial Toxin, Pyocyanin J. Immunol., March 1, 2008; 180(5): 3502 - 3511. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. M. Bianchi, L. R. Prince, K. McPhillips, L. Allen, H. M. Marriott, G. W. Taylor, P. G. Hellewell, I. Sabroe, D. H. Dockrell, P. W. Henson, et al. Impairment of Apoptotic Cell Engulfment by Pyocyanin, a Toxic Metabolite of Pseudomonas aeruginosa Am. J. Respir. Crit. Care Med., January 1, 2008; 177(1): 35 - 43. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 E. J. Naylor, D. Bakstad, M. Biffen, B. Thong, P. Calverley, S. Scott, C. A. Hart, R. J. Moots, and S. W. Edwards Haemophilus influenzae Induces Neutrophil Necrosis: A Role in Chronic Obstructive Pulmonary Disease? Am. J. Respir. Cell Mol. Biol., August 1, 2007; 37(2): 135 - 143. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. Jia, Y. Wang, L. Zhou, and S. Jin Expression of Pseudomonas aeruginosa Toxin ExoS Effectively Induces Apoptosis in Host Cells Infect. Immun., December 1, 2006; 74(12): 6557 - 6570. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. H. Dockrell and M. K. B. Whyte Regulation of phagocyte lifespan in the lung during bacterial infection J. Leukoc. Biol., May 1, 2006; 79(5): 904 - 908. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
I. Nagaoka, H. Tamura, and M. Hirata An Antimicrobial Cathelicidin Peptide, Human CAP18/LL-37, Suppresses Neutrophil Apoptosis via the Activation of Formyl-Peptide Receptor-Like 1 and P2X7. J. Immunol., March 1, 2006; 176(5): 3044 - 3052. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
B. Mehrad, S. J. Park, G. Akangire, T. J. Standiford, T. Wu, J. Zhu, and C. Mohan The lupus-susceptibility locus, sle3, mediates enhanced resistance to bacterial infections. J. Immunol., March 1, 2006; 176(5): 3233 - 3239. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
