Unlike other pathologies, inflammation is a condition that all individuals experience in their lives. Toothache, sunburn, a twisted ankle or cutting your hand while slicing bread, they all evoke what we call an acute inflammatory response. This type of response normally displays the cardinal signs of inflammation originally described by Aulus Cornelius Celsus: redness, swelling, heat and pain. Acute inflammation does not normally require any therapeutic intervention other than perhaps a painkiller, as it resolves, with the damage being naturally repaired. Inflammation is also at the root of many other diseases in a more ‘silent’ way as the cardinal signs of inflammation are not so evident. It is now appreciated that inflammatory mechanisms and processes contribute to the pathogenesis of a number of conditions including obesity, cancer, rheumatoid arthritis, atherosclerosis and diabetes. These are examples of chronic inflammation, arising either by the persistence of the injurious element causing it, or by a defect in our endogenous natural protective mechanisms grouped under the terminology of pro-resolving mechanisms. A common perception, likely to have been enhanced by the large variety of nonprescription antiinflammatory drugs available to anyone experiencing mild-to-moderate pain, is that inflammation is something harmful that must be stopped. In the next sections we will discuss on the protective life-saving role of the inflammatory response, the existence of our own body's resolutive mechanisms that regulate it and on when and why we need a pharmacological intervention to treat inflammation.
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August 01 2017
Resolution in an ‘over-inflamed’ era Free
Mauro Perretti;
Mauro Perretti
1Queen Mary University of London, UK
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Trinidad MonteroMelendez
Trinidad MonteroMelendez
1Queen Mary University of London, UK
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Publisher: Portland Press Ltd
Online ISSN: 1740-1194
Print ISSN: 0954-982X
2017 © Biochemical Society
2017
Biochem (Lond) (2017) 39 (4): 4–7.
Citation
Mauro Perretti, Trinidad MonteroMelendez; Resolution in an ‘over-inflamed’ era. Biochem (Lond) 1 August 2017; 39 (4): 4–7. doi: https://doi.org/10.1042/BIO03904004
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