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Study of organ injury and appropriat...

Craciun, Florin Lucian.

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Study of organ injury and appropriate treatment of sepsis in a murine model using prediction and monitoring biomarkers.

Record Type:	Language materials, printed : Monograph/item
Title/Author:	Study of organ injury and appropriate treatment of sepsis in a murine model using prediction and monitoring biomarkers./
Author:	Craciun, Florin Lucian.
Description:	232 p.
Notes:	Source: Dissertation Abstracts International, Volume: 72-04, Section: B, page: 2045.
Contained By:	Dissertation Abstracts International72-04B.
Subject:	Health Sciences, Pathology. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3445682
ISBN:	9781124491325

Study of organ injury and appropriate treatment of sepsis in a murine model using prediction and monitoring biomarkers.
Craciun, Florin Lucian.

Study of organ injury and appropriate treatment of sepsis in a murine model using prediction and monitoring biomarkers. - 232 p.

Source: Dissertation Abstracts International, Volume: 72-04, Section: B, page: 2045.

Thesis (Ph.D.)--Boston University, 2011.

Neutrophils are critical for the rapid eradication of bacterial pathogens, but they may also contribute to the development of multiple organ failure in sepsis. We hypothesized that increasing early recruitment of neutrophils to the focus of infection will increase bacterial clearance and improve survival without inducing organ injury. The murine cecal ligation and puncture (CLP) induced sepsis model was used. A plasma biomarker, interleukin 6 (IL-6), was used to predict survival after sepsis. A new protocol with two different discrimination values was developed to more accurately predict 5-day survival (Live-P) or death (Die-P). Long-term daily collection of a small blood sample from the facial vein proved to be a safe monitoring tool for septic mice. Using the biomarker, the development of organ injury in Live-P and Die-P mice was examined, starting with the lung, which fails most frequently in sepsis. Despite increased pulmonary inflammation, there was no increased recruitment of neutrophils to the lung, pulmonary edema or histologic damage in Die-P mice, eliminating lung injury as cause of death. While no histological alterations were found, Die-P mice had diminished renal function as indicated by plasma urea and cystatin C levels. The liver and pancreas were not injured in Die-P. The local (peritoneal) neutrophil recruitment and bacterial presence were examined next. Live-P and Die-P mice had similar peritoneal neutrophil recruitment 6 hours post-CLP fighting nearly identical bacterial loads. In Die-P mice peritoneal bacteria numbers increased between 6 and 24 hours post-CLP, while in Live-P they decreased. We tested next if increasing early local neutrophil recruitment would eradicate the bacteria and improve survival. When given immediately after CLP, exogenous CXC chemokines increased peritoneal neutrophil recruitment at 6 hours post-CLP. This early increase in neutrophils induced by exogenous chemokines resulted in significantly fewer peritoneal bacteria by 24 hours and a significantly improved 28 day survival. The window of opportunity for the treatment is short as when given 6 hours post-CLP the chemokines did not improve survival. These data demonstrate that early, local treatment with CXC chemokines enhances neutrophil recruitment, clearance of bacteria and improves survival in the CLP model of sepsis.

ISBN: 9781124491325Subjects--Topical Terms:

1017854
Health Sciences, Pathology.

Study of organ injury and appropriate treatment of sepsis in a murine model using prediction and monitoring biomarkers.
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500 $a Adviser: Daniel Remick.
502 $a Thesis (Ph.D.)--Boston University, 2011.
520 $a Neutrophils are critical for the rapid eradication of bacterial pathogens, but they may also contribute to the development of multiple organ failure in sepsis. We hypothesized that increasing early recruitment of neutrophils to the focus of infection will increase bacterial clearance and improve survival without inducing organ injury. The murine cecal ligation and puncture (CLP) induced sepsis model was used. A plasma biomarker, interleukin 6 (IL-6), was used to predict survival after sepsis. A new protocol with two different discrimination values was developed to more accurately predict 5-day survival (Live-P) or death (Die-P). Long-term daily collection of a small blood sample from the facial vein proved to be a safe monitoring tool for septic mice. Using the biomarker, the development of organ injury in Live-P and Die-P mice was examined, starting with the lung, which fails most frequently in sepsis. Despite increased pulmonary inflammation, there was no increased recruitment of neutrophils to the lung, pulmonary edema or histologic damage in Die-P mice, eliminating lung injury as cause of death. While no histological alterations were found, Die-P mice had diminished renal function as indicated by plasma urea and cystatin C levels. The liver and pancreas were not injured in Die-P. The local (peritoneal) neutrophil recruitment and bacterial presence were examined next. Live-P and Die-P mice had similar peritoneal neutrophil recruitment 6 hours post-CLP fighting nearly identical bacterial loads. In Die-P mice peritoneal bacteria numbers increased between 6 and 24 hours post-CLP, while in Live-P they decreased. We tested next if increasing early local neutrophil recruitment would eradicate the bacteria and improve survival. When given immediately after CLP, exogenous CXC chemokines increased peritoneal neutrophil recruitment at 6 hours post-CLP. This early increase in neutrophils induced by exogenous chemokines resulted in significantly fewer peritoneal bacteria by 24 hours and a significantly improved 28 day survival. The window of opportunity for the treatment is short as when given 6 hours post-CLP the chemokines did not improve survival. These data demonstrate that early, local treatment with CXC chemokines enhances neutrophil recruitment, clearance of bacteria and improves survival in the CLP model of sepsis.
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