Sepsis is primarily described as a state of disrupted inflammatory homeostasis that is often initiated by infection. Severe sepsis is organ failure in the setting of sepsis and septic shock is organ failure where sepsis is hypotensive. Bacteria (such as LPS) is used to induce sepsis, setting off an immune response activating immune cells that excrete cytokines.


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Endotoxemia/Lipopolysaccharide (LPS)

Endotoxin or lipopolysaccharide (LPS), the principal component of the out membrane of Gram (-) bacteria, can stimulate the release of inflammatory mediators from various cell types, responsible for initiating the process of sepsis, including increase of pro-inflammatory cytokines, such as TNF-α, IL-1, IL-6 and IL-8. This model is highly reproducible, easy to monitor by a variety of endpoints, and closely mimics clinical sepsis. 


Sepsis can be induced by caecum-ligation and puncture (CLP). Routine treatment will include painkillers, antibiotics and fluid resuscitation (in addition to the evaluation of the test drug). Endpoints include cardiac function (echocardiography), renal function (urea/creatine), liver injury (ALT/AST) and lung inflammation. This model is very established and reproducible.


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Please contact us for more information on any of these models, to obtain a proposal or to arrange to speak with one of our scientists.


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