Cellular processes in XXXX .

@entity1 @entity32 @entity295 @entity326 @entity39 @entity281 @entity881
@entity295 , the systemic inflammatory response to an @entity281 , is an increasingly common condition. It represents a major healthcare problem as affected @entity1 have a high morbidity and mortality leading to high direct and indirect costs. This article describes the progression from a simple @entity281 to @entity326 and @entity881 , 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, @entity295 is characterised by a lack of tissue @entity39 and the ability of most - if not all - organs to recover completely. This underlines the assumption that organ dysfunction during @entity295 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 @entity1 and may represent a state analogous to hibernation, which can be reversed once the @entity281 is overcome and @entity32 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.
