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MedWire News: Acne vulgaris patients are unable to suppress early inflammatory changes due to defective immunosurveillance resulting from low levels of the anti-inflammatory interleukin (IL)-10, say researchers.
“Acne vulgaris is a very common dermatosis characterised by an inflammatory reaction in the pilosebaceous follicles of the face and trunk,” explain Adrian Mountford (University of York, UK) and co-workers.
One trigger for acne is thought to be dysregulation of the inflammatory response to the bacterium Propionibacterium acnes. In normal skin this is prevented by the action of factors such as IL-10, which is a “strong inhibitor of IL-12 production in the skin and likely acts to contain excessive dermal inflammation.”
The team investigated the response of peripheral blood mononuclear cells (PBMCs) cultured from 47 acne patients and 40 age- and gender-matched controls to stimulation with P. acnes.
As reported in the British Journal of Dermatology, Mountford and colleagues found that pro-inflammatory factors such as IL-8 and tumor necrosis factor (TNF)-α were higher in PBMCs taken from acne patients compared with those from controls.
However, cells taken from acne patients secreted significantly lower amounts of IL-10 compared with those from controls.
The impaired IL-10 production was isolated to CD14+ cells thought to be monocytes. The researchers found that CD14 cells from acne patients were unable to destroy P. acnes, but function appeared to be restored on addition of IL-10.
Mountford and team conclude that “acne therapeutics might profitably target IL-10 both as a regulator of pro-inflammatory cytokines and in augmenting the CD14+ cell phagocytic response.”
They add: “Future studies should seek to characterize the cellular sources of IL-10 in evolving and healing acne lesions and compare the skin distribution of IL-10 in subjects with acne and subjects who acne has spontaneously resolved.”
MedWire (www.medwire-news.md) is an independent clinical news service provided by Current Medicine Group, a part of Springer Science+Business Media. © Current Medicine Group Ltd; 2009