A short comment is appropriate in this section. Many of the anti-inflammatory drugs (i.e. antibiotics and benzoyl peroxide) used in acne may work predominantly against P. acnes but  there is  some evidence that  they  can modulate    inflammation    by   nonmicrobiological methods.

Polymorphonucleocytes incubated with autologous serum samples from patients receiving tetracycline hydrochloride (1 g/day) demonstrated significant acne inflammation. Lymphocytes are the initial  cell type in most papules, with polymorphonucleocytes having an important, but phase 2, response. Chemotaxis of polymorphonucleocytes has been shown to be due to P. acnes, especially its lipase, and a substance of MW <2,000 KD. Other   comedonal  contents  of  nonbacteriological origin may be important. Stimulation of both the alternate and classical pathways are also central to  acne inflammation.  P. acnes  cell wall  is a potent activator but other comedonal contents could be important. Late-stage  acne  inflammation is a  nonspecific macrophage and, at times, giant cell  response. Healing may be complete with regeneration of the pilosebaceous follicle but at times scarring is the result.