Pseudomonas pyocyanin inhibits wound repair by inducing premature cellular senescence: Role for p38 mitogen-activated protein kinase

Abstract Pseudomonas aeruginosa is an important nosocomial pathogen of burn wounds. Pyocyanin, a virulence factor produced by the bacterium, induces persistent intracellular oxidative stress and premature senescence in mammalian cells. Our aims were to evaluate pyocyanin levels in infected wound dre...

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Published inBurns Vol. 35; no. 4; pp. 500 - 508
Main Authors Muller, Michael, Li, Zhe, Maitz, Peter K.M
Format Journal Article
LanguageEnglish
Published Kidlington Elsevier Ltd 01.06.2009
Elsevier
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Abstract Abstract Pseudomonas aeruginosa is an important nosocomial pathogen of burn wounds. Pyocyanin, a virulence factor produced by the bacterium, induces persistent intracellular oxidative stress and premature senescence in mammalian cells. Our aims were to evaluate pyocyanin levels in infected wound dressings and the potential of the toxin to influence wound repair. Surgical dressings from infected burn patients were examined for pyocyanin and normal primary human diploid fibroblasts (HDFs) were treated with comparable concentrations and their replicative ability examined. Pyocyanin was detected in the exudate of infected wound dressings in amounts up to 5.3 μg/g (mean: 2.0 ± 2.3 μg/g). HDFs exposed to pyocyanin (1–50 μM; 0.2–10.5 μg/ml) underwent growth arrest at all concentrations and developed morphological characteristics associated with cellular senescence, including expression of senescence-associated β-galactosidase. Using an in vitro wound repair model, a single exposure to pyocyanin inhibited wound repair in a concentration-dependent manner. Prior treatment with a specific p38MAPK inhibitor allowed cells to maintain their replicative ability and pre-senescent morphology indicating pyocyanin operates through the Erk/p38MAPK senescence pathway. These data support the hypothesis that bacterial virulence factors capable of inducing persistent low-level oxidative stress play a pivotal role in modulating the tissue repair response to infection by inducing premature cellular senescence.
AbstractList Pseudomonas aeruginosa is an important nosocomial pathogen of burn wounds. Pyocyanin, a virulence factor produced by the bacterium, induces persistent intracellular oxidative stress and premature senescence in mammalian cells. Our aims were to evaluate pyocyanin levels in infected wound dressings and the potential of the toxin to influence wound repair. Surgical dressings from infected burn patients were examined for pyocyanin and normal primary human diploid fibroblasts (HDFs) were treated with comparable concentrations and their replicative ability examined. Pyocyanin was detected in the exudate of infected wound dressings in amounts up to 5.3 mu g/g (mean: 2.0 +/- 2.3 mu g/g). HDFs exposed to pyocyanin (1-50 mu M; 0.2-10.5 mu g/ml) underwent growth arrest at all concentrations and developed morphological characteristics associated with cellular senescence, including expression of senescence-associated beta -galactosidase. Using an in vitro wound repair model, a single exposure to pyocyanin inhibited wound repair in a concentration-dependent manner. Prior treatment with a specific p38 super(MAPK) inhibitor allowed cells to maintain their replicative ability and pre-senescent morphology indicating pyocyanin operates through the Erk/p38 super(MAPK) senescence pathway. These data support the hypothesis that bacterial virulence factors capable of inducing persistent low-level oxidative stress play a pivotal role in modulating the tissue repair response to infection by inducing premature cellular senescence.
Pseudomonas aeruginosa is an important nosocomial pathogen of burn wounds. Pyocyanin, a virulence factor produced by the bacterium, induces persistent intracellular oxidative stress and premature senescence in mammalian cells. Our aims were to evaluate pyocyanin levels in infected wound dressings and the potential of the toxin to influence wound repair. Surgical dressings from infected burn patients were examined for pyocyanin and normal primary human diploid fibroblasts (HDFs) were treated with comparable concentrations and their replicative ability examined. Pyocyanin was detected in the exudate of infected wound dressings in amounts up to 5.3 microg/g (mean: 2.0+/-2.3 microg/g). HDFs exposed to pyocyanin (1-50 microM; 0.2-10.5 microg/ml) underwent growth arrest at all concentrations and developed morphological characteristics associated with cellular senescence, including expression of senescence-associated beta-galactosidase. Using an in vitro wound repair model, a single exposure to pyocyanin inhibited wound repair in a concentration-dependent manner. Prior treatment with a specific p38(MAPK) inhibitor allowed cells to maintain their replicative ability and pre-senescent morphology indicating pyocyanin operates through the Erk/p38(MAPK) senescence pathway. These data support the hypothesis that bacterial virulence factors capable of inducing persistent low-level oxidative stress play a pivotal role in modulating the tissue repair response to infection by inducing premature cellular senescence.
Abstract Pseudomonas aeruginosa is an important nosocomial pathogen of burn wounds. Pyocyanin, a virulence factor produced by the bacterium, induces persistent intracellular oxidative stress and premature senescence in mammalian cells. Our aims were to evaluate pyocyanin levels in infected wound dressings and the potential of the toxin to influence wound repair. Surgical dressings from infected burn patients were examined for pyocyanin and normal primary human diploid fibroblasts (HDFs) were treated with comparable concentrations and their replicative ability examined. Pyocyanin was detected in the exudate of infected wound dressings in amounts up to 5.3 μg/g (mean: 2.0 ± 2.3 μg/g). HDFs exposed to pyocyanin (1–50 μM; 0.2–10.5 μg/ml) underwent growth arrest at all concentrations and developed morphological characteristics associated with cellular senescence, including expression of senescence-associated β-galactosidase. Using an in vitro wound repair model, a single exposure to pyocyanin inhibited wound repair in a concentration-dependent manner. Prior treatment with a specific p38MAPK inhibitor allowed cells to maintain their replicative ability and pre-senescent morphology indicating pyocyanin operates through the Erk/p38MAPK senescence pathway. These data support the hypothesis that bacterial virulence factors capable of inducing persistent low-level oxidative stress play a pivotal role in modulating the tissue repair response to infection by inducing premature cellular senescence.
Pseudomonas aeruginosa is an important nosocomial pathogen of burn wounds. Pyocyanin, a virulence factor produced by the bacterium, induces persistent intracellular oxidative stress and premature senescence in mammalian cells. Our aims were to evaluate pyocyanin levels in infected wound dressings and the potential of the toxin to influence wound repair. Surgical dressings from infected burn patients were examined for pyocyanin and normal primary human diploid fibroblasts (HDFs) were treated with comparable concentrations and their replicative ability examined. Pyocyanin was detected in the exudate of infected wound dressings in amounts up to 5.3 μg/g (mean: 2.0 ± 2.3 μg/g). HDFs exposed to pyocyanin (1–50 μM; 0.2–10.5 μg/ml) underwent growth arrest at all concentrations and developed morphological characteristics associated with cellular senescence, including expression of senescence-associated β-galactosidase. Using an in vitro wound repair model, a single exposure to pyocyanin inhibited wound repair in a concentration-dependent manner. Prior treatment with a specific p38 MAPK inhibitor allowed cells to maintain their replicative ability and pre-senescent morphology indicating pyocyanin operates through the Erk/p38 MAPK senescence pathway. These data support the hypothesis that bacterial virulence factors capable of inducing persistent low-level oxidative stress play a pivotal role in modulating the tissue repair response to infection by inducing premature cellular senescence.
Author Li, Zhe
Maitz, Peter K.M
Muller, Michael
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Issue 4
Keywords Wound repair
Oxidative stress
Pyocyanin
Cellular senescence
Tissue remodeling
Mitogen-activated protein kinase
Pseudomonas aeruginosa
Burns
Fibroblast
Pseudomonadales
Premature
Skin disease
Senescence
Enzyme
Transferases
Wound
Burn
Bacteria
Pseudomonadaceae
Repair
Language English
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Snippet Abstract Pseudomonas aeruginosa is an important nosocomial pathogen of burn wounds. Pyocyanin, a virulence factor produced by the bacterium, induces persistent...
Pseudomonas aeruginosa is an important nosocomial pathogen of burn wounds. Pyocyanin, a virulence factor produced by the bacterium, induces persistent...
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SubjectTerms Bandages - microbiology
beta-Galactosidase - analysis
Biological and medical sciences
Burns
Burns - complications
Burns - microbiology
Cell Proliferation
Cells, Cultured
Cellular senescence
Cellular Senescence - drug effects
Critical Care
Fibroblast
Fibroblasts - drug effects
Fibroblasts - physiology
Humans
Medical sciences
Mitogen-activated protein kinase
Oxidative stress
Oxidative Stress - drug effects
p38 Mitogen-Activated Protein Kinases - pharmacology
Pseudomonas aeruginosa
Pseudomonas aeruginosa - pathogenicity
Pseudomonas Infections - microbiology
Pseudomonas Infections - prevention & control
Pyocyanin
Pyocyanine - adverse effects
Pyocyanine - analysis
Tissue remodeling
Traumas. Diseases due to physical agents
Virulence
Virulence Factors - adverse effects
Wound Healing - drug effects
Wound Healing - physiology
Wound repair
Title Pseudomonas pyocyanin inhibits wound repair by inducing premature cellular senescence: Role for p38 mitogen-activated protein kinase
URI https://www.clinicalkey.es/playcontent/1-s2.0-S0305417908003598
https://dx.doi.org/10.1016/j.burns.2008.11.010
https://www.ncbi.nlm.nih.gov/pubmed/19286324
https://search.proquest.com/docview/21029429
https://search.proquest.com/docview/733327059
Volume 35
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