author_facet Khan, Momina
Patrick, Amanda L.
Fox-Robichaud, Alison E.
Translational Biology Group, The Canadian Critical Care
Khan, Momina
Patrick, Amanda L.
Fox-Robichaud, Alison E.
Translational Biology Group, The Canadian Critical Care
author Khan, Momina
Patrick, Amanda L.
Fox-Robichaud, Alison E.
Translational Biology Group, The Canadian Critical Care
spellingShingle Khan, Momina
Patrick, Amanda L.
Fox-Robichaud, Alison E.
Translational Biology Group, The Canadian Critical Care
BioMed Research International
Development of a Murine Model of Early Sepsis in Diet-Induced Obesity
General Immunology and Microbiology
General Biochemistry, Genetics and Molecular Biology
General Medicine
author_sort khan, momina
spelling Khan, Momina Patrick, Amanda L. Fox-Robichaud, Alison E. Translational Biology Group, The Canadian Critical Care 2314-6133 2314-6141 Hindawi Limited General Immunology and Microbiology General Biochemistry, Genetics and Molecular Biology General Medicine http://dx.doi.org/10.1155/2014/719853 <jats:p>Sepsis, a global health issue, is the most common cause of mortality in the intensive care unit. The aim of this study was to develop a new model of sepsis that investigates the impact of prolonged western diet (WD) induced obesity on the response to early sepsis. Male C57BL/6 mice were fed either a high fat WD or normal chow diet (NCD) for 6, 15, or 27 weeks. Septic obese mice at 15 and 27 weeks had significantly lower levels of lung myeloperoxidase (26.3 ± 3.80 U/mg tissue) compared to age matched ad lib (44.1 ± 2.86 U/mg tissue) and diet restricted (63.2 ± 5.60 U/mg tissue) controls. Low levels of lung inflammation were not associated with changes in hepatic cytokines and oxidative stress levels. Obese mice had significantly (<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" id="M1"><mml:mi>P</mml:mi><mml:mo>&lt;</mml:mo><mml:mn fontstyle="italic">0.0001</mml:mn></mml:math>) larger livers compared to controls. Histological examination of the livers demonstrated that WD fed mice had increased inflammation with pronounced fat infiltration, steatosis, and hepatocyte ballooning. Using this model of prolonged exposure to high fat diet we have data that agree with recent clinical observations suggesting obese individuals are protected from sepsis-induced lung injury. This model will allow us to investigate the links between damage to the hepatic microcirculation, immune response, and lung injury.</jats:p> Development of a Murine Model of Early Sepsis in Diet-Induced Obesity BioMed Research International
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title Development of a Murine Model of Early Sepsis in Diet-Induced Obesity
title_unstemmed Development of a Murine Model of Early Sepsis in Diet-Induced Obesity
title_full Development of a Murine Model of Early Sepsis in Diet-Induced Obesity
title_fullStr Development of a Murine Model of Early Sepsis in Diet-Induced Obesity
title_full_unstemmed Development of a Murine Model of Early Sepsis in Diet-Induced Obesity
title_short Development of a Murine Model of Early Sepsis in Diet-Induced Obesity
title_sort development of a murine model of early sepsis in diet-induced obesity
topic General Immunology and Microbiology
General Biochemistry, Genetics and Molecular Biology
General Medicine
url http://dx.doi.org/10.1155/2014/719853
publishDate 2014
physical 1-11
description <jats:p>Sepsis, a global health issue, is the most common cause of mortality in the intensive care unit. The aim of this study was to develop a new model of sepsis that investigates the impact of prolonged western diet (WD) induced obesity on the response to early sepsis. Male C57BL/6 mice were fed either a high fat WD or normal chow diet (NCD) for 6, 15, or 27 weeks. Septic obese mice at 15 and 27 weeks had significantly lower levels of lung myeloperoxidase (26.3 ± 3.80 U/mg tissue) compared to age matched ad lib (44.1 ± 2.86 U/mg tissue) and diet restricted (63.2 ± 5.60 U/mg tissue) controls. Low levels of lung inflammation were not associated with changes in hepatic cytokines and oxidative stress levels. Obese mice had significantly (<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" id="M1"><mml:mi>P</mml:mi><mml:mo>&lt;</mml:mo><mml:mn fontstyle="italic">0.0001</mml:mn></mml:math>) larger livers compared to controls. Histological examination of the livers demonstrated that WD fed mice had increased inflammation with pronounced fat infiltration, steatosis, and hepatocyte ballooning. Using this model of prolonged exposure to high fat diet we have data that agree with recent clinical observations suggesting obese individuals are protected from sepsis-induced lung injury. This model will allow us to investigate the links between damage to the hepatic microcirculation, immune response, and lung injury.</jats:p>
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author Khan, Momina, Patrick, Amanda L., Fox-Robichaud, Alison E., Translational Biology Group, The Canadian Critical Care
author_facet Khan, Momina, Patrick, Amanda L., Fox-Robichaud, Alison E., Translational Biology Group, The Canadian Critical Care, Khan, Momina, Patrick, Amanda L., Fox-Robichaud, Alison E., Translational Biology Group, The Canadian Critical Care
author_sort khan, momina
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description <jats:p>Sepsis, a global health issue, is the most common cause of mortality in the intensive care unit. The aim of this study was to develop a new model of sepsis that investigates the impact of prolonged western diet (WD) induced obesity on the response to early sepsis. Male C57BL/6 mice were fed either a high fat WD or normal chow diet (NCD) for 6, 15, or 27 weeks. Septic obese mice at 15 and 27 weeks had significantly lower levels of lung myeloperoxidase (26.3 ± 3.80 U/mg tissue) compared to age matched ad lib (44.1 ± 2.86 U/mg tissue) and diet restricted (63.2 ± 5.60 U/mg tissue) controls. Low levels of lung inflammation were not associated with changes in hepatic cytokines and oxidative stress levels. Obese mice had significantly (<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" id="M1"><mml:mi>P</mml:mi><mml:mo>&lt;</mml:mo><mml:mn fontstyle="italic">0.0001</mml:mn></mml:math>) larger livers compared to controls. Histological examination of the livers demonstrated that WD fed mice had increased inflammation with pronounced fat infiltration, steatosis, and hepatocyte ballooning. Using this model of prolonged exposure to high fat diet we have data that agree with recent clinical observations suggesting obese individuals are protected from sepsis-induced lung injury. This model will allow us to investigate the links between damage to the hepatic microcirculation, immune response, and lung injury.</jats:p>
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spelling Khan, Momina Patrick, Amanda L. Fox-Robichaud, Alison E. Translational Biology Group, The Canadian Critical Care 2314-6133 2314-6141 Hindawi Limited General Immunology and Microbiology General Biochemistry, Genetics and Molecular Biology General Medicine http://dx.doi.org/10.1155/2014/719853 <jats:p>Sepsis, a global health issue, is the most common cause of mortality in the intensive care unit. The aim of this study was to develop a new model of sepsis that investigates the impact of prolonged western diet (WD) induced obesity on the response to early sepsis. Male C57BL/6 mice were fed either a high fat WD or normal chow diet (NCD) for 6, 15, or 27 weeks. Septic obese mice at 15 and 27 weeks had significantly lower levels of lung myeloperoxidase (26.3 ± 3.80 U/mg tissue) compared to age matched ad lib (44.1 ± 2.86 U/mg tissue) and diet restricted (63.2 ± 5.60 U/mg tissue) controls. Low levels of lung inflammation were not associated with changes in hepatic cytokines and oxidative stress levels. Obese mice had significantly (<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" id="M1"><mml:mi>P</mml:mi><mml:mo>&lt;</mml:mo><mml:mn fontstyle="italic">0.0001</mml:mn></mml:math>) larger livers compared to controls. Histological examination of the livers demonstrated that WD fed mice had increased inflammation with pronounced fat infiltration, steatosis, and hepatocyte ballooning. Using this model of prolonged exposure to high fat diet we have data that agree with recent clinical observations suggesting obese individuals are protected from sepsis-induced lung injury. This model will allow us to investigate the links between damage to the hepatic microcirculation, immune response, and lung injury.</jats:p> Development of a Murine Model of Early Sepsis in Diet-Induced Obesity BioMed Research International
spellingShingle Khan, Momina, Patrick, Amanda L., Fox-Robichaud, Alison E., Translational Biology Group, The Canadian Critical Care, BioMed Research International, Development of a Murine Model of Early Sepsis in Diet-Induced Obesity, General Immunology and Microbiology, General Biochemistry, Genetics and Molecular Biology, General Medicine
title Development of a Murine Model of Early Sepsis in Diet-Induced Obesity
title_full Development of a Murine Model of Early Sepsis in Diet-Induced Obesity
title_fullStr Development of a Murine Model of Early Sepsis in Diet-Induced Obesity
title_full_unstemmed Development of a Murine Model of Early Sepsis in Diet-Induced Obesity
title_short Development of a Murine Model of Early Sepsis in Diet-Induced Obesity
title_sort development of a murine model of early sepsis in diet-induced obesity
title_unstemmed Development of a Murine Model of Early Sepsis in Diet-Induced Obesity
topic General Immunology and Microbiology, General Biochemistry, Genetics and Molecular Biology, General Medicine
url http://dx.doi.org/10.1155/2014/719853