1. ¹INSERM, U563, Centre de Physiopathologie de Toulouse Purpan, Toulouse, France
2. ²Centre de Recherche Pierre Fabre CERPER, Toulouse, France
3. ³Unité de dermatologie pédiatrique, Hôpital Pellegrin-Enfants, Université de Bordeaux 2–Victor Segalen, Bordeaux, France
4. ⁴Service de dermatologie et Unité de dermatologie pédiatrique, Hôpitaux St André et Pellegrin-Enfants, CHU de Bordeaux, Bordeaux, France
5. ⁵INSERM E217, Université Bordeaux 2–Victor Segalen, Bordeaux, France

Correspondence: Dr Christian Davrinche, INSERM, U563, Centre de Physiopathologie de Toulouse Purpan, Toulouse F-31300, France. E-mail: davrinch@toulouse.inserm.fr

Received 24 January 2007; Revised 9 July 2007; Accepted 15 August 2007; Published online 25 October 2007.

Abstract

As shown by atopy patch tests, atopic dermatitis (AD) is dominated in its acute phase by the development of a specific T_H2 response after exposure of the skin to common environmental antigens. Relying on our previous data showing that Staphylococcus aureus enterotoxin B (SEB) induced the activation of monocyte-derived dendritic cells (DCs) through Toll-like receptor (TLR)2 and that SEB-pulsed DCs commit allogenic naive T cells into T_H2, we assessed monocytes sensitivity to SEB and lipopolysaccharide (LPS) in a group of children and adult patients with AD. Monocytes from AD patients (15 adults with mostly severe disease and 15 children with mild to moderate disease) exhibited an activated and tolerant state as supported by (i) secretion of large amounts of IL-6, IL-10, and tumor necrosis factor- even in the absence of stimulation; (ii) their inability to modulate neither HLA-DR and CD54 nor TLR2 and TLR4 expression after in vitro challenge with SEB; (iii) inhibition of IL-12p70 secretion in response to LPS. Interestingly, monocytes from some of the children studied responded to in vitro challenge with LPS, suggesting new hypotheses to explain disease regression. Our data support the notion that monitoring sensitivity of monocytes to bacterial toxins could prove useful to assess disease progression and prognosis in AD.