The Role of Interleukin-10 During Systemic Inflammation and Bacterial Infection
Sepsis is a clinical syndrome that results from a systemic response of the host to an infection. Activation of several host inflammatory mediator systems, including the cytokine network, is considered to play an important role in the pathogenesis of sepsis. Cytokines are a family of small proteins which function in a complex network in which they can influence each other’s production and activity. Pro-inflammatory cytokines, of which tumour necrosis factor-α(TNF) and interleukin-1 (IL-1) are studied most extensively, stimulate inflammatory processes and facilitate the immune response against invading pathogens. However, excessive systemic release of pro-inflammatory cytokines during sepsis syndrome has been found to contribute to the development of tissue damage. The production of these pro-inflammatory cytokines can be inhibited by so-called anti-inflammatory cytokines. The prototype of this group of mediators is IL-10. In this article we will discuss the role of IL-10 in the pathogenesis of sepsis and severe bacterial infections.
KeywordsMajor Histocompatibility Complex Systemic Inflammation Staphylococcal Enterotoxin Severe Bacterial Infection Clinical Sepsis
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