The body's initial response to a pro-inflammatory insult is to release mediators like tumour necrosis factor (TNF), interleukin 1, interleukin 6, and platelet-activating factor (PAF). These mediators have multiple overlapping effects designed to repair existing damage and limit new damage. To ensure that the effects of the pro-inflammatory mediators do not become destructive, the body then launches compensatory anti-inflammatory mediators like interleukin 4 and interleukin 10, which downregulate the initial pro-inflammatory response. In severe sepsis, regulation of the early response to a pro-inflammatory insult is lost and a massive systemic reaction occurs with excessive or inappropriate inflammatory reactions, resulting in the development of diffuse capillary injury.
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