Abstract
A massive production of inflammatory cytokines, such as tumor necrosis factor (TNF), interleukin-1 (IL-1) and interferon-γ (IFN-γ) occurs in conditions such as sepsis and infectious diseases. This cytokine overproduction can have deleterious effects on various organs, including lungs, liver or brain. One of the major target cells of inflammatory cytokines is the microvascular endothelial cell (MVEC), that is both morphologically and functionally different from large vessel endothelial cells (Table 1). Apart from being sensitive towards the direct cytotoxicity of some of the inflammatory cytokines such as TNF, activated MVEC can also stimulate and attract leukocytes, via the production of chemokines, and regulate their extravasation into tissues. We will review the direct and indirect effects of TNF on endothelial cells that can be relevant for the pathogenesis of septic shock, with particular attention to acute respiratory distress syndrome (ARDS), and cerebral malaria.
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Keywords
- Septic Shock
- Acute Respiratory Distress Syndrome
- Cerebral Malaria
- Tumor Necrosis Factor Receptor
- Adult Respiratory Distress Syndrome
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Lucas, R., Suter, P.M., Grau, G.E. (1997). TNF in Septic Shock and Cerebral Malaria. In: Vincent, JL. (eds) Yearbook of Intensive Care and Emergency Medicine 1997. Yearbook of Intensive Care and Emergency Medicine, vol 1997. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-662-13450-4_6
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DOI: https://doi.org/10.1007/978-3-662-13450-4_6
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