Abstract
Inflammation was first described in history by Cornelius Celsus (30 BC–38 AD) as a process that embraces “rubor et tumor cum calore et dolore”, i.e. redness and swelling accompanied by heat and pain. Inflammation is the result of a series of enzymatic processes in the body. Cell membrane damage caused by a cut or scratch, for example, leads to the activation of phospholipases, which mediate the release of arachidonic acid. This metabolite is further processed by cyclooxy-genases and lipoxygenases to produce the fever-causing prostaglandins, thromboxanes and leukotrienes. These fatty acid derivatives have a vasodilatory action, causing a higher blood flow to help attracting inflammatory cytokines and immune cells to the site of inflammation. This explains the accompanying symptoms of redness and swelling in inflamed tissue. The inflammation process is further mediated and controlled by the action of several messenger molecules called cytokines, chemokines and adhesion molecules, including TNF, IL-1, IL-2, IL-6, MCP-1, IL-8, GM-CSF, ICAM-1 and E-selectin (Cato & Wade, 1996; Barnes & Karin, 1997). These cytokines are produced by (and in turn activate) different surrounding cell types, such as fibroblasts, endothelial cells (lining blood vessels), macrophages and neutrophils, white blood cell components traveling through the bloodstream.
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De Bosscher, K., Vanden Berghe, W., Haegeman, G. (2003). Regulation of NF-кB by Glucocorticoids. In: Beyaert, R. (eds) Nuclear Factor кB. Springer, Dordrecht. https://doi.org/10.1007/978-94-010-0163-2_10
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