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C. acnes also provokes skin inflammation by altering the fatty composition of oily sebum. Oxidation of the lipid squalene by C. acnes is of particular importance. Squalene oxidation activates NF-κB (a protein complex) and consequently increases IL-1α levels. Additionally, squalene oxidation leads to increased activity of the 5-lipoxygenase enzyme responsible for conversion of arachidonic acid to leukotriene B4 (LTB4). LTB4 promotes skin inflammation by acting on the peroxisome proliferator-activated receptor alpha (PPARα) protein. PPARα increases activity of activator protein 1 (AP-1) and NF-κB, thereby leading to the recruitment of inflammatory T cells. The inflammatory properties of C. acnes can be further explained by the bacterium's ability to convert sebum triglycerides to pro-inflammatory free fatty acids via secretion of the enzyme lipase. These free fatty acids spur production of cathelicidin, HBD1, and HBD2, thus leading to further inflammation.
Pimples are raised red spots with a white center that develop when blocked hair follicles become inflamed or infected with bacteria. Blockages and inflammation that develop deep inside hair follicles produce cystlike lumps beneath the surface of your skin. Other pores in your skin, which are the openings of the sweat glands, aren't usually involved in acne.