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Cellular processes in sepsis


Rudiger, A; Stotz, M; Singer, M (2008). Cellular processes in sepsis. Swiss Medical Weekly, 138(43–44):629-634.

Abstract

Sepsis, the systemic inflammatory response to an infection, is an increasingly common condition. It represents a major healthcare problem as affected patients have a high morbidity and mortality leading to high direct and indirect costs. This article describes the progression from a simple infection to septic shock and multi-organ failure, with a special emphasis on the body’s response at the cellular level.
Pathogen recognition by the host is followed by a cascade of pro- and anti-inflammatory mediators that attempt to defend the body and prevent further harm. Both pathogen virulence and host resistance regulate the severity of the inflammatory response. As a result of the inflammatory insult, mitochondria are damaged functionally and structurally. Since mitochondria are responsible for intracellular energy production, mitochondrial dysfunction places the cells at risk of developing energy failure and, consequently, cell death. However, sepsis is characterised by a lack of tissue necrosis and the ability of most – if not all – organs to recover completely. This underlines the assumption that organ dysfunction during sepsis is predominantly a functional problem which appears to relate to the creation of a new balance between energy generation and expenditure. Hence, organ dysfunction could be viewed as a protective mechanism for the patient and may represent a state analogous to hibernation, which can be reversed once the infection is overcome and inflammation has abated. More research is needed to develop better directed and timed therapeutic interventions that can reduce the high morbidity and mortality of this common condition.

Sepsis, the systemic inflammatory response to an infection, is an increasingly common condition. It represents a major healthcare problem as affected patients have a high morbidity and mortality leading to high direct and indirect costs. This article describes the progression from a simple infection to septic shock and multi-organ failure, with a special emphasis on the body’s response at the cellular level.
Pathogen recognition by the host is followed by a cascade of pro- and anti-inflammatory mediators that attempt to defend the body and prevent further harm. Both pathogen virulence and host resistance regulate the severity of the inflammatory response. As a result of the inflammatory insult, mitochondria are damaged functionally and structurally. Since mitochondria are responsible for intracellular energy production, mitochondrial dysfunction places the cells at risk of developing energy failure and, consequently, cell death. However, sepsis is characterised by a lack of tissue necrosis and the ability of most – if not all – organs to recover completely. This underlines the assumption that organ dysfunction during sepsis is predominantly a functional problem which appears to relate to the creation of a new balance between energy generation and expenditure. Hence, organ dysfunction could be viewed as a protective mechanism for the patient and may represent a state analogous to hibernation, which can be reversed once the infection is overcome and inflammation has abated. More research is needed to develop better directed and timed therapeutic interventions that can reduce the high morbidity and mortality of this common condition.

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22 citations in Web of Science®
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Additional indexing

Item Type:Journal Article, refereed, further contribution
Communities & Collections:04 Faculty of Medicine > University Hospital Zurich > Clinic and Policlinic for Internal Medicine
Dewey Decimal Classification:610 Medicine & health
Language:German
Date:2008
Deposited On:03 Mar 2009 10:27
Last Modified:05 Apr 2016 13:08
Publisher:EMH Swiss Medical Publishers
ISSN:0036-7672
Additional Information:Free full text article
Official URL:http://www.smw.ch/docs/pdf200x/2008/43/smw-12319.pdf
Related URLs:http://www.smw.ch/docs/archive200x/2008/43/smw-12319.html (Publisher)
PubMed ID:19005868
Permanent URL: http://doi.org/10.5167/uzh-17139

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