Biofilm-forming Pseudomonas aeruginosa bacteria undergo lipopolysaccharide structural modifications and induce enhanced inflammatory cytokine response in human monocytes.
To determine whether growth of bacteria in biofilms triggers a specific immune response, we compared cytokine induction in human monocytes and mouse macrophages by planktonic and biofilm bacteria. We compared Pseudomonas aeruginosa and Staphylococcus aureus, two bacteria often colonizing the airways of cystic fibrosis patients. Planktonic and biofilm S. aureus induced equivalent amounts of cytokine in human monocytes. In contrast, biofilm-forming P. aeruginosa induced a higher production of tumor necrosis factor and interleukin-6 than their planktonic counterpart, both for clinical isolates and laboratory strains. This increased cytokine production was partly dependent on phagocytosis. In contrast, no difference in cytokine induction was observed with mouse macrophages. We investigated the structures of the lipopolysaccharides (LPSs) of these Gram-negative bacteria in biofilm and planktonic cultures of P. aeruginosa. Switch between the two life-styles was shown to cause several reversible LPS structure modifications affecting the lipid A and polysaccharide moieties of both clinical isolates and laboratory strains. In addition, LPS isolated from biofilm-grown bacteria induced slightly more inflammatory cytokines than that extracted from its planktonic counterpart. Our results, therefore, show that P. aeruginosa biofilm LPS undergoes structural modifications that only partially contribute to an increased inflammatory response from human monocytes.
Ciornei
Cristina D
CD
Unité Cytokines & Inflammation, Institut Pasteur, Paris, France. jean-marc.cavaillon@pasteur.fr
Novikov
Alexey
A
Beloin
Christophe
C
Fitting
Catherine
C
Caroff
Martine
M
Ghigo
Jean-Marc
JM
Cavaillon
Jean-Marc
JM
Adib-Conquy
Minou
M
D000818:Animals; D018441:Biofilms / Q000254:growth & development; D002478:Cells, Cultured; D006801:Humans; D018836:Inflammation Mediators / Q000378:metabolism; D015850:Interleukin-6 / Q000378:metabolism; D008070:Lipopolysaccharides / Q000737:chemistry / Q000378:metabolism*; D008168:Lung / Q000276:immunology / Q000378:metabolism* / Q000382:microbiology / Q000473:pathology; D008264:Macrophages / Q000276:immunology / Q000378:metabolism* / Q000382:microbiology / Q000473:pathology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D015394:Molecular Structure; D009000:Monocytes / Q000276:immunology / Q000378:metabolism* / Q000382:microbiology / Q000473:pathology; D011550:Pseudomonas aeruginosa / Q000502:physiology*; D013211:Staphylococcus aureus / Q000502:physiology*
D018836:Inflammation Mediators; D015850:Interleukin-6; D008070:Lipopolysaccharides