Chronic Pseudomonas aeruginosa biofilm infection impairs murine S100A8/A9 and neutrophil effector cytokines—implications for delayed wound closure?

Research output: Contribution to journal › Journal article › Research › peer-review

Standard

Chronic Pseudomonas aeruginosa biofilm infection impairs murine S100A8/A9 and neutrophil effector cytokines—implications for delayed wound closure? / Trøstrup, Hannah; Lerche, Christian Johann; Christophersen, Lars Jackie; Thomsen, Kim; Jensen, Peter Østrup; Hougen, Hans Petter; Høiby, Niels; Moser, Claus.

In: Pathogens and Disease, Vol. 75, No. 7, ftx068, 10.2017.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Trøstrup, H, Lerche, CJ, Christophersen, LJ, Thomsen, K, Jensen, PØ, Hougen, HP, Høiby, N & Moser, C 2017, 'Chronic Pseudomonas aeruginosa biofilm infection impairs murine S100A8/A9 and neutrophil effector cytokines—implications for delayed wound closure?', Pathogens and Disease, vol. 75, no. 7, ftx068. https://doi.org/10.1093/femspd/ftx068

APA

Trøstrup, H., Lerche, C. J., Christophersen, L. J., Thomsen, K., Jensen, P. Ø., Hougen, H. P., Høiby, N., & Moser, C. (2017). Chronic Pseudomonas aeruginosa biofilm infection impairs murine S100A8/A9 and neutrophil effector cytokines—implications for delayed wound closure? Pathogens and Disease, 75(7), [ftx068]. https://doi.org/10.1093/femspd/ftx068

Vancouver

Trøstrup H, Lerche CJ, Christophersen LJ, Thomsen K, Jensen PØ, Hougen HP et al. Chronic Pseudomonas aeruginosa biofilm infection impairs murine S100A8/A9 and neutrophil effector cytokines—implications for delayed wound closure? Pathogens and Disease. 2017 Oct;75(7). ftx068. https://doi.org/10.1093/femspd/ftx068

Author

Trøstrup, Hannah ; Lerche, Christian Johann ; Christophersen, Lars Jackie ; Thomsen, Kim ; Jensen, Peter Østrup ; Hougen, Hans Petter ; Høiby, Niels ; Moser, Claus. / Chronic Pseudomonas aeruginosa biofilm infection impairs murine S100A8/A9 and neutrophil effector cytokines—implications for delayed wound closure?. In: Pathogens and Disease. 2017 ; Vol. 75, No. 7.

Bibtex

@article{609265801e064ed58c81401fd749b518,
title = "Chronic Pseudomonas aeruginosa biofilm infection impairs murine S100A8/A9 and neutrophil effector cytokines—implications for delayed wound closure?",
abstract = "The impact of Pseudomonas aeruginosa biofilm infections in chronic wounds and clinical implication for healing is receiving increased attention. However, the pathophysiology of host/pathogen interplay is not fully understood. By further revealing the mechanisms, necessary new treatment strategies may be identified. Since the background for chronic wounds is diverse, representative animal models are important. We assessed host response and spontaneous wound closure in the relatively resistant C3H/HeN and the susceptible BALB/c mouse strain. Full-thickness burn wounds were inflicted in 108 mice. P. aeruginosa biofilm (106 colony forming units) was injected subcutaneously in 72 mice, euthanized day 4, 7 or 10 days postinfection. Wounds were analysed for neutrophil host response markers: S100A8/A9, keratinocyte-derived chemokine and Granulocyte-Colony Stimulating Factor. Total peripheral blood leukocyte and polymorphonuclear count were assessed in parallel. Histopathology evaluated wound inflammatory burden. Photoplanimetry described macroscopical wound closure. Stable chronic wound infection was established in all challenged mice. P. aeruginosa biofilm suppressed neutrophil host response in wounds. C3H/HeN mice achieved earlier systemic inflammatory control and healed faster than BALB/c mice. P. aeruginosa biofilms perturbs host defense thereby inducing a steady-state of chronic infection which may impair wound healing. These results indicate therapeutic options for immune modulation of biofilm-infected wounds.",
author = "Hannah Tr{\o}strup and Lerche, {Christian Johann} and Christophersen, {Lars Jackie} and Kim Thomsen and Jensen, {Peter {\O}strup} and Hougen, {Hans Petter} and Niels H{\o}iby and Claus Moser",
note = "Erratum: https://doi.org/10.1093/femspd/ftx110",
year = "2017",
month = oct,
doi = "10.1093/femspd/ftx068",
language = "English",
volume = "75",
journal = "FEMS Immunology and Medical Microbiology",
issn = "2049-632X",
publisher = "Oxford University Press",
number = "7",

}

RIS

TY - JOUR

T1 - Chronic Pseudomonas aeruginosa biofilm infection impairs murine S100A8/A9 and neutrophil effector cytokines—implications for delayed wound closure?

AU - Trøstrup, Hannah

AU - Lerche, Christian Johann

AU - Christophersen, Lars Jackie

AU - Thomsen, Kim

AU - Jensen, Peter Østrup

AU - Hougen, Hans Petter

AU - Høiby, Niels

AU - Moser, Claus

N1 - Erratum: https://doi.org/10.1093/femspd/ftx110

PY - 2017/10

Y1 - 2017/10

N2 - The impact of Pseudomonas aeruginosa biofilm infections in chronic wounds and clinical implication for healing is receiving increased attention. However, the pathophysiology of host/pathogen interplay is not fully understood. By further revealing the mechanisms, necessary new treatment strategies may be identified. Since the background for chronic wounds is diverse, representative animal models are important. We assessed host response and spontaneous wound closure in the relatively resistant C3H/HeN and the susceptible BALB/c mouse strain. Full-thickness burn wounds were inflicted in 108 mice. P. aeruginosa biofilm (106 colony forming units) was injected subcutaneously in 72 mice, euthanized day 4, 7 or 10 days postinfection. Wounds were analysed for neutrophil host response markers: S100A8/A9, keratinocyte-derived chemokine and Granulocyte-Colony Stimulating Factor. Total peripheral blood leukocyte and polymorphonuclear count were assessed in parallel. Histopathology evaluated wound inflammatory burden. Photoplanimetry described macroscopical wound closure. Stable chronic wound infection was established in all challenged mice. P. aeruginosa biofilm suppressed neutrophil host response in wounds. C3H/HeN mice achieved earlier systemic inflammatory control and healed faster than BALB/c mice. P. aeruginosa biofilms perturbs host defense thereby inducing a steady-state of chronic infection which may impair wound healing. These results indicate therapeutic options for immune modulation of biofilm-infected wounds.

AB - The impact of Pseudomonas aeruginosa biofilm infections in chronic wounds and clinical implication for healing is receiving increased attention. However, the pathophysiology of host/pathogen interplay is not fully understood. By further revealing the mechanisms, necessary new treatment strategies may be identified. Since the background for chronic wounds is diverse, representative animal models are important. We assessed host response and spontaneous wound closure in the relatively resistant C3H/HeN and the susceptible BALB/c mouse strain. Full-thickness burn wounds were inflicted in 108 mice. P. aeruginosa biofilm (106 colony forming units) was injected subcutaneously in 72 mice, euthanized day 4, 7 or 10 days postinfection. Wounds were analysed for neutrophil host response markers: S100A8/A9, keratinocyte-derived chemokine and Granulocyte-Colony Stimulating Factor. Total peripheral blood leukocyte and polymorphonuclear count were assessed in parallel. Histopathology evaluated wound inflammatory burden. Photoplanimetry described macroscopical wound closure. Stable chronic wound infection was established in all challenged mice. P. aeruginosa biofilm suppressed neutrophil host response in wounds. C3H/HeN mice achieved earlier systemic inflammatory control and healed faster than BALB/c mice. P. aeruginosa biofilms perturbs host defense thereby inducing a steady-state of chronic infection which may impair wound healing. These results indicate therapeutic options for immune modulation of biofilm-infected wounds.

U2 - 10.1093/femspd/ftx068

DO - 10.1093/femspd/ftx068

M3 - Journal article

C2 - 28645160

VL - 75

JO - FEMS Immunology and Medical Microbiology

JF - FEMS Immunology and Medical Microbiology

SN - 2049-632X

IS - 7

M1 - ftx068

ER -

ID: 179847641