Extracellular DNA: a major proinflammatory component of Pseudomonas aeruginosa biofilms

We previously demonstrated that extracellular bacterial DNA activates neutrophils through a CpG- and TLR9-independent mechanism. Biofilms are microbial communities enclosed in a polymeric matrix that play a critical role in the pathogenesis of many infectious diseases. Because extracellular DNA is a...

Full description

Saved in:
Bibliographic Details
Published in:The Journal of immunology (1950) 2010-06, Vol.184 (11), p.6386-6395
Main Authors: Fuxman Bass, Juan I, Russo, Daniela M, Gabelloni, Maria L, Geffner, Jorge R, Giordano, Mirta, Catalano, Mariana, Zorreguieta, Angeles, Trevani, Analía S
Format: Article
Language:English
Subjects:
Biofilms - growth & development
Cytokines - biosynthesis
DNA, Bacterial - immunology
Extracellular Fluid - chemistry
Extracellular Fluid - microbiology
Humans
Microscopy, Confocal
Neutrophil Activation - immunology
Neutrophils - immunology
Neutrophils - metabolism
Pseudomonas aeruginosa - physiology
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:We previously demonstrated that extracellular bacterial DNA activates neutrophils through a CpG- and TLR9-independent mechanism. Biofilms are microbial communities enclosed in a polymeric matrix that play a critical role in the pathogenesis of many infectious diseases. Because extracellular DNA is a key component of biofilms of different bacterial species, the aim of this study was to determine whether it plays a role in the ability of biofilms to induce human neutrophil activation. We found that degradation of matrix extracellular DNA with DNase I markedly reduced the capacity of Pseudomonas aeruginosa biofilms to induce the release of the neutrophil proinflammatory cytokines IL-8 and IL-1beta (>75%); reduced the upregulation of neutrophil activation markers CD18, CD11b, and CD66b (p < 0.001); reduced the number of bacteria phagocytosed per neutrophil contacting the biofilm; and reduced the production of neutrophil extracellular traps. Consistent with these findings, we found that biofilms formed by the lasI rhlI P. aeruginosa mutant strain, exhibiting a very low content of matrix extracellular DNA, displayed a lower capacity to stimulate the release of proinflammatory cytokines by neutrophils, which was not decreased further by DNase I treatment. Together, our findings support that matrix extracellular DNA is a major proinflammatory component of P. aeruginosa biofilms.
ISSN:0022-1767
1550-6606
DOI:10.4049/jimmunol.0901640