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Interleukin-10 secretion from CD14+ peripheral blood mononuclear cells is downregulated in patients with acne vulgaris
British Journal of Dermatology, 10/13/09

Mountford A et al. – The data suggest that patients with acne have a proinflammatory cytokine milieu and crucially are unable to contain early inflammatory changes due to a specific defect in immunosurveillance, namely low monocyte IL–10 production.

Exclusive Author Commentary
Adrian Mountford, 10/14/09

Acne: new suspects, CD14+ mononuclear cells After decades of research, we know a great deal about late events in acne lesion formation. Once visible inflammation is present, multiple inflammatory cascades have already been set in motion and it is difficult, if not impossible to determine, which event came first. When papules and pustules are days old, there is very little to distinguish acne from other types of chronic inflammation associated with delayed-type hypersensitivity responses to persistent immunogens. In order to develop better treatments for acne, that prevent rather than treat the disease, it is necessary to identify the factor(s) that determine acne-proneness or trigger the earliest, potentially reversible, inflammatory changes. This small study has shown that acne patients may have a central defect in IL-10 production by peripheral blood mononuclear cells that makes them incapable of mounting a sufficiently vigorous anti-inflammatory response to minor immunologic stimuli within pilosebaceous follicles where acne lesions develop. Reduced production of IL-10 was shown to be associated with a paucity of CD14+ monocytes/immature macrophages in acne patients compared with age-matched healthy controls. The immunogen used to stimulate monocytes was whole live cells of Propionibacterium acnes, the bacterium implicated in inflammatory acne. IL-10 is the predominant cytokine that dampens down the inflammatory response and over-production in late lesions has been demonstrated. Once inflammation becomes established, up-regulation of IL-10 production may help to resolve existing lesions and cellular sources other than monocytes may contribute to local IL-10 synthesis at this late stage. It is the monocyte that is critical in the earliest stages. Monocytes are vital components of immune surveillance within the skin. They are the first troops on the scene when an inflammatory stimulus is detected. If their response in inadequate, the sub-clinical event is not contained and visible inflammation will ensue. If others confirm this deficit in IL-10 production in acne patients, then we shall be a step closer to identifying the earliest pathogenic changes in acne. However, we still have to address the question as to whether P. acnes is universally present in sub-clinically inflamed follicles or whether the pro-inflammatory stimulus is non-microbial. A key role for IL-1? in acne has long been suspected since Guy and Kealey (Dermatology 1998; 196:32-7) demonstrated that this cytokine alone can trigger comedogenesis. It is present in large amounts in comedones and its release by keratinocytes can be triggered by an injury response, for example, the onset of sebum flow though an immature duct. Whether the defective monocytes are attempting to respond directly to P. acnes or indirectly to IL-1?, the consequences in terms of unchecked inflammation will be similar.

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