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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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These inflammatory mediators will in turn activate the dermal fibroblasts, normally responsible for collagen production as well as cells of the immune system such as mast cells. These cells will produce collagenases and other metalloproteases—a family of enzymes. These enzymes degrade the collagen and other constituents of the extracellular matrix (elastin, hyaluronic acid) to help the migration of immune cells delivered from the lymph nodes to the site of the inflammatory reaction.

Since the activation of the immune response is usually triggered by a bacterial invasion or other types of aggression (chemical pollutants, UV, etc.), the immune cells act to destroy and eliminate the factors that have activated the stress. Remember, this is a non-specific response; pollutants and UV are perceived as invaders because they trigger the same kind of damage in a first phase as bacteria. The elimination of these factors is usually done by producing different types of free radicals, which are highly toxic for bacteria. However, the response activated by the immune cells is generally excessively strong, inducing some severe damage to the healthy cells located nearby the site of injury.

It is easy then to see how low-level irritants, such as pollutants, can trigger an almost ongoing inflammatory reaction that, in the long run, accelerates skin aging.


Recent research on a phenomenon called inflamm-aging is interesting as it really points out chronic inflammation as a major culprit in aging, and brings a new dimension to the understanding of inflammation: that of endogenous inflammation (inflammation caused from within the body).

Inflamm-aging is a phenomenon triggered by the conjunction of chronic repetitive and subclinical inflammation from external aggressors and internal inflammatory mechanisms due to the progressive degradation of systems such as the mitochondrial function.