Conflicts of interestThe authors state no conflict of interest.
Interleukin-10 secretion from CD14+ peripheral blood mononuclear cells is downregulated in patients with acne vulgaris
Article first published online: 20 JUL 2009
© 2009 The Authors. Journal Compilation © 2009 British Association of Dermatologists
British Journal of Dermatology
Volume 162, Issue 2, pages 296–303, February 2010
How to Cite
Caillon, F., O’Connell, M., Eady, E.A., Jenkins, G.R., Cove, J.H., Layton, A.M. and Mountford, A.P. (2010), Interleukin-10 secretion from CD14+ peripheral blood mononuclear cells is downregulated in patients with acne vulgaris. British Journal of Dermatology, 162: 296–303. doi: 10.1111/j.1365-2133.2009.09420.x
- Issue published online: 13 JAN 2010
- Article first published online: 20 JUL 2009
- Accepted for publication 13 July 2009
Background Acne is a common chronic inflammatory dermatosis of the pilosebaceous unit. It is characterized by seborrhoea, comedone formation and an inflammatory response consistent with defective cellular immunity to Propionibacterium acnes.
Objectives The objective of this study was to investigate the immune reactivity of patients with acne compared with healthy controls by examining the response of peripheral blood mononuclear cells (PBMCs) to stimulation with P. acnes. Particular focus was placed upon measuring the production of interleukin (IL)-10, which has an established immunoregulatory role.
Patients and methods Venous blood was collected from 47 patients with acne and 40 age- and sex-matched healthy controls with no prior history of acne. PBMCs were cultured and their cytokine response to P. acnes investigated.
Results Proinflammatory IL-8 and tumour necrosis factor (TNF)-α secretion from PBMCs was higher in patients with acne when stimulated with P. acnes. In contrast, a statistically significant reduction in PBMC secretion of anti-inflammatory IL-10 in patients with acne was identified. The impaired production of IL-10 by PBMCs from patients with acne was confined to CD14+ cells presumed to be monocytes. The ability of CD14 cells from patients with acne to phagocytose P. acnes bacteria was also observed to be defective but the addition of exogenous IL-10 to PBMC cultures restored phagocytic activity.
Conclusions These 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. Our observations raise the possibility that acne therapeutics might profitably target IL-10 both as a regulator of proinflammatory cytokines and in augmenting the CD14+ cell phagocytic response.