Sepsis represents an important infectious process with systemic manifestation. The incidence of sepsis
is continuously increasing. This epidemiologic trend reflects the aging population, increasing number of
chronically ill patients and invasiveness of the modern medicine. An increasing resistance of infectious
agents causing sepsis plays also a role. The progress in diagnosis and treatment of sepsis, which was
achieved in last decades, influenced prognosis of the disease only slightly. This fact is due to our
inadequate understanding of sepsis pathogenesis. An important role in the sepsis pathogenesis is played
by systemic inflammatory response, which may cause tissue damage leading to the organ failure. This
reaction is controlled by anti-inflammatory response, which may be exaggerated leading to increased
susceptibility to secondary infections or reduced ability to combat primary infection. The knowledge
obtained from experimental studies could not been utilized, because of short therapeutic window of new
immunotherapies. As an example is a failure of clinical study with monoclonal antibody against TNF-α.
Thus, the search for new clinically effective therapeutic agents is aimed at pathogenetic mechanisms
activated in longer time frame after the primary insult. Currently, out of drugs modulating the already
known immunopathophysiological mechanisms of sepsis corticosteroids and activated protein C are
sepsis, epidemiology, aetiology, pathogenesis.