Pseudomonas aeruginosa and the hyperlipidaemia of sepsis

Rajkumar Cheluvappa, Gerene M. Denning, Gee Lau, Michael C. Grimm, Sarah N. Hilmer, David G. Le Couteur

Research output: Contribution to journalArticle

Abstract

Pathophysiological alterations of liver sinusoidal endothelial cells (LSECs) impact liver and metabolism. LSEC fenestrations are pores facilitating lipoproteins and macromolecule transfer between blood and hepatocytes. The Gram negative bacterium Pseudomonas aeruginosa is one of the most common opportunistic nosocomial pathogens, especially in post-liver transplant recipients. Gram negative bacterial endotoxin (lipopolysaccharide, LPS) and the P. aeruginosa toxin, pyocyanin, have marked effects on LSECs, including loss of porosity (defenestration). Currently proposed mechanisms for sepsis-hyperlipidaemia, an important response to Gram negative bacterial sepsis, include tissue lipoprotein-lipase inhibition and increased hepatic triglyceride production. Owing to the well-substantiated role of LSECs in liver-allograft rejection and hyperlipidaemia, we propose defenestration of the LSEC is an additional cellular mechanism for sepsis-hyperlipidaemia, including pseudomonal sepsis post-liver transplantation.

Original languageEnglish (US)
Pages (from-to)615-621
Number of pages7
JournalPathology
Volume41
Issue number7
DOIs
StatePublished - Dec 2009

Fingerprint

Hyperlipidemias
Pseudomonas aeruginosa
Sepsis
Liver
Endothelial Cells
Pyocyanine
Lipoprotein Lipase
Porosity
Gram-Negative Bacteria
Endotoxins
Liver Transplantation
Lipoproteins
Allografts
Lipopolysaccharides
Hepatocytes
Triglycerides

Keywords

  • Fenestration
  • Hyperlipidaemia
  • Liver sinusoidal endothelial cell
  • Oxidative stress
  • Pseudomonas aeruginosa
  • Pyocyanin
  • Sepsis
  • Transplantation

ASJC Scopus subject areas

  • Pathology and Forensic Medicine

Cite this

Cheluvappa, R., Denning, G. M., Lau, G., Grimm, M. C., Hilmer, S. N., & Le Couteur, D. G. (2009). Pseudomonas aeruginosa and the hyperlipidaemia of sepsis. Pathology, 41(7), 615-621. https://doi.org/10.3109/00313020903257764

Pseudomonas aeruginosa and the hyperlipidaemia of sepsis. / Cheluvappa, Rajkumar; Denning, Gerene M.; Lau, Gee; Grimm, Michael C.; Hilmer, Sarah N.; Le Couteur, David G.

In: Pathology, Vol. 41, No. 7, 12.2009, p. 615-621.

Research output: Contribution to journalArticle

Cheluvappa, R, Denning, GM, Lau, G, Grimm, MC, Hilmer, SN & Le Couteur, DG 2009, 'Pseudomonas aeruginosa and the hyperlipidaemia of sepsis', Pathology, vol. 41, no. 7, pp. 615-621. https://doi.org/10.3109/00313020903257764
Cheluvappa R, Denning GM, Lau G, Grimm MC, Hilmer SN, Le Couteur DG. Pseudomonas aeruginosa and the hyperlipidaemia of sepsis. Pathology. 2009 Dec;41(7):615-621. https://doi.org/10.3109/00313020903257764
Cheluvappa, Rajkumar ; Denning, Gerene M. ; Lau, Gee ; Grimm, Michael C. ; Hilmer, Sarah N. ; Le Couteur, David G. / Pseudomonas aeruginosa and the hyperlipidaemia of sepsis. In: Pathology. 2009 ; Vol. 41, No. 7. pp. 615-621.
@article{2110dc26e37b43c182eee18b37284d45,
title = "Pseudomonas aeruginosa and the hyperlipidaemia of sepsis",
abstract = "Pathophysiological alterations of liver sinusoidal endothelial cells (LSECs) impact liver and metabolism. LSEC fenestrations are pores facilitating lipoproteins and macromolecule transfer between blood and hepatocytes. The Gram negative bacterium Pseudomonas aeruginosa is one of the most common opportunistic nosocomial pathogens, especially in post-liver transplant recipients. Gram negative bacterial endotoxin (lipopolysaccharide, LPS) and the P. aeruginosa toxin, pyocyanin, have marked effects on LSECs, including loss of porosity (defenestration). Currently proposed mechanisms for sepsis-hyperlipidaemia, an important response to Gram negative bacterial sepsis, include tissue lipoprotein-lipase inhibition and increased hepatic triglyceride production. Owing to the well-substantiated role of LSECs in liver-allograft rejection and hyperlipidaemia, we propose defenestration of the LSEC is an additional cellular mechanism for sepsis-hyperlipidaemia, including pseudomonal sepsis post-liver transplantation.",
keywords = "Fenestration, Hyperlipidaemia, Liver sinusoidal endothelial cell, Oxidative stress, Pseudomonas aeruginosa, Pyocyanin, Sepsis, Transplantation",
author = "Rajkumar Cheluvappa and Denning, {Gerene M.} and Gee Lau and Grimm, {Michael C.} and Hilmer, {Sarah N.} and {Le Couteur}, {David G.}",
year = "2009",
month = "12",
doi = "10.3109/00313020903257764",
language = "English (US)",
volume = "41",
pages = "615--621",
journal = "Pathology",
issn = "0031-3025",
publisher = "Lippincott Williams and Wilkins",
number = "7",

}

TY - JOUR

T1 - Pseudomonas aeruginosa and the hyperlipidaemia of sepsis

AU - Cheluvappa, Rajkumar

AU - Denning, Gerene M.

AU - Lau, Gee

AU - Grimm, Michael C.

AU - Hilmer, Sarah N.

AU - Le Couteur, David G.

PY - 2009/12

Y1 - 2009/12

N2 - Pathophysiological alterations of liver sinusoidal endothelial cells (LSECs) impact liver and metabolism. LSEC fenestrations are pores facilitating lipoproteins and macromolecule transfer between blood and hepatocytes. The Gram negative bacterium Pseudomonas aeruginosa is one of the most common opportunistic nosocomial pathogens, especially in post-liver transplant recipients. Gram negative bacterial endotoxin (lipopolysaccharide, LPS) and the P. aeruginosa toxin, pyocyanin, have marked effects on LSECs, including loss of porosity (defenestration). Currently proposed mechanisms for sepsis-hyperlipidaemia, an important response to Gram negative bacterial sepsis, include tissue lipoprotein-lipase inhibition and increased hepatic triglyceride production. Owing to the well-substantiated role of LSECs in liver-allograft rejection and hyperlipidaemia, we propose defenestration of the LSEC is an additional cellular mechanism for sepsis-hyperlipidaemia, including pseudomonal sepsis post-liver transplantation.

AB - Pathophysiological alterations of liver sinusoidal endothelial cells (LSECs) impact liver and metabolism. LSEC fenestrations are pores facilitating lipoproteins and macromolecule transfer between blood and hepatocytes. The Gram negative bacterium Pseudomonas aeruginosa is one of the most common opportunistic nosocomial pathogens, especially in post-liver transplant recipients. Gram negative bacterial endotoxin (lipopolysaccharide, LPS) and the P. aeruginosa toxin, pyocyanin, have marked effects on LSECs, including loss of porosity (defenestration). Currently proposed mechanisms for sepsis-hyperlipidaemia, an important response to Gram negative bacterial sepsis, include tissue lipoprotein-lipase inhibition and increased hepatic triglyceride production. Owing to the well-substantiated role of LSECs in liver-allograft rejection and hyperlipidaemia, we propose defenestration of the LSEC is an additional cellular mechanism for sepsis-hyperlipidaemia, including pseudomonal sepsis post-liver transplantation.

KW - Fenestration

KW - Hyperlipidaemia

KW - Liver sinusoidal endothelial cell

KW - Oxidative stress

KW - Pseudomonas aeruginosa

KW - Pyocyanin

KW - Sepsis

KW - Transplantation

UR - http://www.scopus.com/inward/record.url?scp=72749112787&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=72749112787&partnerID=8YFLogxK

U2 - 10.3109/00313020903257764

DO - 10.3109/00313020903257764

M3 - Article

C2 - 20001339

AN - SCOPUS:72749112787

VL - 41

SP - 615

EP - 621

JO - Pathology

JF - Pathology

SN - 0031-3025

IS - 7

ER -