Elsevier

Clinics in Dermatology

Volume 22, Issue 5, September–October 2004, Pages 380-384
Clinics in Dermatology

Acne: Inflammation

https://doi.org/10.1016/j.clindermatol.2004.03.006Get rights and content

Abstract

The inflammatory stage of acne vulgaris is usually of greatest concern to the patient. A number of morphologically different inflammatory lesions may form that can be painful and unsightly. In 30% of patients, such lesions lead to scarring.1 Inflammatory acne and acne scarring can have significant psychological effects on the patient, including depression, anxiety, and poor self-image.2 Although inflammatory acne has been well characterized clinically, the mechanisms by which inflammatory lesions arise are still poorly understood. The human skin commensal bacterium, Propionibacterium acnes, has long been associated with inflammatory acne. This organism has been implicated over and above all of the other cutaneous microflora in contributing to the inflammatory response characteristic of acne. However, its precise role in the disease and its interaction with the human immune system remain to be elucidated.

Section snippets

P. acnes and acne

acnes has been implicated in the pathogenesis of acne for more than 100 years. It was initially believed to be the direct cause of the disease when it was first isolated in 1896, and subsequent studies demonstrating an inflammatory response after injection of P. acnes into the skin reinforced this view.3, 4 However, these findings were cast into doubt when the organism was shown to reside on normal human skin 50 years later.5 The association between P. acnes and acne has been reaffirmed over

Development of inflammatory lesions: comedogenesis

Inflammatory lesions develop from comedones arising due to an abnormal pattern of keratinization in the sebaceous follicle.1 Comedogenesis was once thought to not be part of the inflammatory process, but detailed immunohistological studies that have followed the development of inflammatory acne lesions have shown this to be the first step toward formation of an inflammatory lesion. The microcomedone is now believed to be the earliest type of subclinical acne lesion.

Microcomedones develop into

Inflammation: Sequence of events

Debate over the initial cellular infiltrate in inflammatory acne lesions has continued since the first histological studies were carried out 30–40 years ago. Results of some of the first studies concluded that the lymphocyte was the initiating inflammatory cell type.20, 21, 22 However, Kligman's 1974 study10 concluded that there was an initial infiltrate of neutrophils followed by microscopic rupture of the sebaceous follicle wall and subsequent formation of a clinically visible inflamed

The role of p. acnes in inflammation

P. acnes has been shown to be associated with inflammatory acne through antibiotic resistance studies.6, 8 However, this bacterium has not been shown to be a direct cause of the disease or to be involved in the initiation of inflammation. Numbers of viable bacteria within follicles show no correlation with severity of inflammation, and some inflamed lesions do not contain viable P. acnes.29 However, nonviable P. acnes cells are immunostimulatory.30 P. acnes produces a number of enzymes and

Hypotheses and perspectives

The spontaneous resolution of acne is one of the most intriguing features of the disease, and any hypothesis concerning the pathogenesis of acne must attempt to provide an explanation for this event. There is now strong evidence that inflammation in acne is initiated by a specific CD4+ T-cell response. The lymphocytic infiltrate observed in early inflammatory lesions could be due to specific recruitment of T cells. Changes in the follicle microenvironment may lead to an increase in the

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