Abstract :
[en] Sepsis, severe sepsis and septic shock were thought to be provoked by an overwhelming
inflammation in response to an infectious process. This was documented in several animal
studies. However, in human sepsis, excess of inflammation is hard to be observed. Compartimentalization
of the host response rather favors a systemic anti-inflammatory climate. Clinical
situations are complex: on one hand, virulence factors of microorganisms can directly harm the
host tissues, divert the defence mechanisms or distract the control mechanisms of the host,
preventing the normal interaction of endogenous mediators. On the other hand, septic shock
mostly occurs in patients experiencing previous organic or functional vital failures before the
development of infection. The vulnerability of the patient appears therefore to be a key point
in the severity of the disease. Enhancing the host defence mechanisms rather than inhibiting
the inflammatory reaction may become a preferential option.
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