Fructooligosacharides reduce Pseudomonas aeruginosa PAO1 pathogenicity through distinct mechanisms.
Pseudomonas aeruginosa is ubiquitously present in the environment and acts as an opportunistic pathogen on humans, animals and plants. We report here the effects of the prebiotic polysaccharide inulin and its hydrolysed form FOS on this bacterium. FOS was found to inhibit bacterial growth of strain PAO1, while inulin did not affect growth rate or yield in a significant manner. Inulin stimulated biofilm formation, whereas a dramatic reduction of the biofilm formation was observed in the presence of FOS. Similar opposing effects were observed for bacterial motility, where FOS inhibited the swarming and twitching behaviour whereas inulin caused its stimulation. In co-cultures with eukaryotic cells (macrophages) FOS and, to a lesser extent, inulin reduced the secretion of the inflammatory cytokines IL-6, IL-10 and TNF-α. Western blot experiments indicated that the effects mediated by FOS in macrophages are associated with a decreased activation of the NF-κB pathway. Since FOS and inulin stimulate pathway activation in the absence of bacteria, the FOS mediated effect is likely to be of indirect nature, such as via a reduction of bacterial virulence. Further, this modulatory effect is observed also with the highly virulent ptxS mutated strain. Co-culture experiments of P. aeruginosa with IEC18 eukaryotic cells showed that FOS reduces the concentration of the major virulence factor, exotoxin A, suggesting that this is a possible mechanism for the reduction of pathogenicity. The potential of these compounds as components of antibacterial and anti-inflammatory cocktails is discussed.
Department of Biochemistry and Molecular Biology II, Centre of networked Biomedical Research about Hepatic and Digestive Diseases, School of Pharmacy, University of Granada, Granada, Spain.
Mercedes
M
Ortega-González
Departments of Pharmacology, Centre of networked Biomedical Research about Hepatic and Digestive Diseases, School of Pharmacy, University of Granada, Granada, Spain.
Fermín
F
Sánchez de Medina
Department of Environmental Protection, Consejo Superior de Investigaciones Científicas, C/Profesor Albareda 1, Granada, Spain.
Carlos
C
Molina-Santiago
Departments of Pharmacology, Centre of networked Biomedical Research about Hepatic and Digestive Diseases, School of Pharmacy, University of Granada, Granada, Spain.
Rocío
R
López-Posadas
Department of Environmental Protection, Consejo Superior de Investigaciones Científicas, C/Profesor Albareda 1, Granada, Spain.
Daniel
D
Pacheco
Department of Environmental Protection, Consejo Superior de Investigaciones Científicas, C/Profesor Albareda 1, Granada, Spain.
Tino
T
Krell
Department of Biochemistry and Molecular Biology II, Centre of networked Biomedical Research about Hepatic and Digestive Diseases, School of Pharmacy, University of Granada, Granada, Spain.
Olga
O
Martínez-Augustin
Department of Environmental Protection, Consejo Superior de Investigaciones Científicas, C/Profesor Albareda 1, Granada, Spain.
Daddaoua
D
Abdelali
D036002:ADP Ribose Transferases / Q000378:metabolism; D000818:Animals; D001426:Bacterial Proteins / Q000235:genetics / Q000378:metabolism; D001427:Bacterial Toxins / Q000378:metabolism; D018441:Biofilms / Q000187:drug effects* / Q000254:growth & development; D015153:Blotting, Western; D002460:Cell Line; D002478:Cells, Cultured; D016207:Cytokines / Q000378:metabolism*; D004268:DNA-Binding Proteins / Q000235:genetics / Q000378:metabolism; D004847:Epithelial Cells / Q000187:drug effects / Q000378:metabolism / Q000382:microbiology; D005098:Exotoxins / Q000378:metabolism; D005260:Female; D007328:Insulin / Q000494:pharmacology; D016753:Interleukin-10 / Q000378:metabolism; D015850:Interleukin-6 / Q000378:metabolism; D008264:Macrophages / Q000187:drug effects* / Q000378:metabolism / Q000382:microbiology; D009154:Mutation; D016328:NF-kappa B / Q000378:metabolism; D009844:Oligosaccharides / Q000494:pharmacology*; D011550:Pseudomonas aeruginosa / Q000187:drug effects* / Q000235:genetics / Q000472:pathogenicity; D051381:Rats; D017208:Rats, Wistar; D015398:Signal Transduction / Q000187:drug effects; D014157:Transcription Factors / Q000235:genetics / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D014774:Virulence / Q000235:genetics; D037521:Virulence Factors / Q000378:metabolism; D000097668:Pseudomonas aeruginosa Exotoxin A
D036002:ADP Ribose Transferases; D001426:Bacterial Proteins; D001427:Bacterial Toxins; D016207:Cytokines; D004268:DNA-Binding Proteins; D005098:Exotoxins; D007328:Insulin; D016753:Interleukin-10; D015850:Interleukin-6; D016328:NF-kappa B; D009844:Oligosaccharides; D014157:Transcription Factors; D014409:Tumor Necrosis Factor-alpha; D037521:Virulence Factors; D000097668:Pseudomonas aeruginosa Exotoxin A; C113064:PtxS protein, Pseudomonas aeruginosa; C120489:oligofructose; C073470:LysR protein, Bacteria