Staphylococcus aureus-specific skin resident memory T cells protect against bacteria colonization but exacerbate atopic dermatitis-like flares in mice.

BACKGROUND: The contribution of Staphylococcus aureus to the exacerbation of atopic dermatitis (AD) is widely documented, but its role as a primary trigger of AD skin symptoms remains poorly explored. OBJECTIVES: This study sought to reappraise the main bacterial factors and underlying immune mechanisms by which S aureus triggers AD-like inflammation. METHODS: This study capitalized on a preclinical model, in which different clinical isolates were applied in the absence of any prior experimental skin injury. RESULTS: The development of S aureus-induced dermatitis depended on the nature of the S aureus strain, its viability, the concentration of the applied bacterial suspension, the production of secreted and nonsecreted factors, as well as the activation of accessory gene regulatory quorum sensing system. In addition, the rising dermatitis, which exhibited the well-documented AD cytokine signature, was significantly inhibited in inflammasome adaptor apoptosis-associated speck-like protein containing a CARD domain- and monocyte/macrophage-deficient animals, but not in T- and B-cell-deficient mice, suggesting a major role for the innate response in the induction of skin inflammation. However, bacterial exposure generated a robust adaptive immune response against S aureus, and an accumulation of S aureus-specific γδ and CD4+ tissue resident memory T cells at the site of previous dermatitis. The latter both contributed to worsen the flares of AD-like dermatitis on new bacteria exposures, but also, protected the mice from persistent bacterial colonization. CONCLUSIONS: These data highlight the induction of unique AD-like inflammation, with the generation of proinflammatory but protective tissue resident memory T cells in a context of natural exposure to pathogenic S aureus strains.

Methylisothiazolinone allergic contact dermatitis: Assessment of relapses in 139 patients after avoidance advice.

BACKGROUND: Methylisothiazolinone (MI) is a preservative that is responsible for an epidemic of allergic contact dermatitis (ACD). Few studies have been published on the prognosis of patients with MI-induced ACD. OBJECTIVES: To evaluate relapses of MI-induced ACD and difficulties in avoiding MI in patients who had received avoidance advice. METHODS: A retrospective study of patients with MI-induced ACD diagnosed in two specialized dermato-allergology units between 2010 and 2015 was performed. The median follow-up was 3 years. RESULTS: Relapses were observed in 64% of 139 included patients, and were severe in 18%. Rinse-off cosmetics were responsible for the largest proportion of relapses (27%). The median time to relapse was 5 months. Sixty-nine per cent of relapses were on the hands, and 29% were on the face. Risk factors for relapsing were hand eczema and a personal history of atopy. The main difficulties encountered in the avoidance strategy were hidden sources of MI, the lack of labelling on industrial products, the complexity of cosmetic labelling, and remembering the name of the allergen. CONCLUSION: MI-induced ACD has a poor prognosis. Its high rate of relapse is mainly attributable to the difficulties of avoidance. Management needs to be improved. Specialized follow-up in the year following diagnosis is essential to educate patients.