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Inflammation and Aging

By: Marie Alice Dibon, PharmD
Posted: March 7, 2011, from the March 2011 issue of GCI Magazine.

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Inflammation is a quick response; not a finely crafted one. It could be compared to a carpet bombing—destroying the enemy with certainty but definitely indiscriminately damaging the sites on which it takes place. Even when the detected enemy is not properly eliminated by the inflammatory response, the damage is still done.

For the most part, however, it does the job. Most times, the damage done as a result of the process of inflammation is in no way comparable to the damage that would be done by the aggressor it is fighting.

When these aggressors are detected, the skin cells—fibroblasts and keratinocytes as well as cells of the immune system such as neutrophils and mast cells—generate substances called inflammatory mediators.

Immune cells, such as T cells and macrophages, are attracted to the site of the aggression by the mediators secreted in the first place: IL1 (interleukine 1) and TNF, for instance, are also called cytokines, and they trigger the migration of the cells. “Cyto” comes from the Greek kutos for cell; “kine” from the Greek kinesis, movement.

There is purpose in the mediators—including IL6, IL10 and prostaglandines such as the prostaglandine E2 (PGE2), for example—increasing blood flow to help the migration of cells and the quick elimination of waste products generated by the reaction. The macrophages also produce nitrous oxide, which increases the blood flow further.