Is acne an XXXX of blocked pilosebaceous follicles? Implications for antimicrobial treatment.

@entity1 @entity75 @entity406 @entity2348 @entity5478 @entity281 @entity56
A model is proposed which is based on the assumption that acne is due to @entity281 of functionally blocked pilosebaceous follicles by propionibacteria. @entity75 , which are first visible during the adrenarche in acne-prone individuals, do not contain propionibacteria. Comedogenesis appears to be independent of @entity2348 and may be driven by high levels of bioactive interleukin-1 alpha derived from ductal hyperkeratinocytes. The stimulus which triggers interleukin-1 alpha production is unknown. @entity406 killed @entity5478 failed to stimulate production of the cytokine by cultured @entity1 keratinocytes in vitro. @entity75 are thought to arise from microcomedones, but the initiating events are unknown. Evidence that propionibacteria are involved in the generation of inflammatory lesions is inconclusive. The cellular infiltrate is consistent with a type IV @entity56 response to one or more persistent lesional antigens, not necessarily bacterial. The potent adjuvant activity of @entity5478 would up-regulate the immune response to any antigen which came into contact with the mononuclear cell infiltrate. Antibiotics are widely used in the treatment of acne, and their effects in selecting a predominantly resistant commensal population are well recognized. Although they reduce numbers of propionibacteria on the skin, other modes of action may contribute to or explain their therapeutic efficacy. At a time when there is global concern that antibiotic resistance rates in common bacterial pathogens may threaten our future ability to control @entity2348 , practices which promote the spread of antibiotic-resistant bacteria must be fully justified. A thorough reappraisal of the role of propionibacteria in acne is overdue. It is likely that further experimental work is needed to confirm or refute that @entity5478 is aptly named.
