Abstract
The production of pro-inflammatory cytokines is a prerequisite for initiating the anti-infectious process, whereas their exacerbated production during severe inflammation may contribute to deleterious consequences. The capacity of interleukin (IL)-l and tumor necrosis factor-alpha (TNF-a) to induce inflammatory mediators contributes to their pro-inflammatory properties. Phospholipase, cyclooxygenase and lipoxygenase are activated by IL-1 and TNF-a leading to the release of prostaglandins, thromboxane, leukotrienes, and platelet activating factor (PAF). Free radicals (superoxide [O 2− ], nitric oxide [NO]), and proteolytic enzymes are other mediators produced by target cells in response to IL-1 and TNF-a. Other cytokines, including chemokines such as IL-8 or some T-cell derived cytokines, such as lymphotoxin-α are also involved in the cytokine cascade (Fig. 1). Different experimental approaches have demonstrated the contribution of the pro-inflammatory cytokines to the harmful effects observed in sepsis, trauma, burns, hemorrhage, severe surgery and other pathophysiological situations leading to systemic inflammatory response syndrome (SIRS). The injection of recombinant pro-inflammatory cytokines mimics some of the clinical parameters observed in SIRS patients and the use of anti-cytokine antibodies prevents most of the deleterious effects observed in animal models of SIRS.
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Keywords
- Proinflammatory Cytokine
- Systemic Inflammatory Response Syndrome
- Acute Phase Protein
- Multiple Organ Dysfunction Syndrome
- Endotoxic Shock
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.
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Cavaillon, JM., Adib-Conquy, M. (2002). The Pro-Inflammatory Cytokine Cascade. In: Marshall, J.C., Cohen, J. (eds) Immune Response in the Critically Ill. Update in Intensive Care Medicine, vol 31. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-57210-4_4
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