Fifty percent of all those with atopic dermatitis develop other allergic symptoms within their first year of life and probably as many as 85% of patients experience an onset below 5 years of age Key insights Atopic dermatitis often begins in early childhood and is the first Key WordsAtopic dermatitis · Atopic march · Skin barrier defect · Immune dysregulation · Genetics · Environment Abstract Atopic dermatitis (AD) is a chronic inflammatory skin disease posing a significant burden on health-care resources and patients' quality of life. It is a complex disease with a wide spectrum of clinical presentations and combinations of symptoms. AD affects up to 20% of children and up to 3% of adults; recent data show that its prevalence is still increasing, especially in low-income countries. First manifestations of AD usually appear early in life and often precede other allergic diseases such as asthma or allergic rhinitis. Individuals affected by AD usually have genetically determined risk factors affecting the skin barrier function or the immune system. However, genetic mutations alone might not be enough to cause clinical manifestations of AD, and it is merely the interaction of a dysfunctional epidermal barrier in genetically predisposed individuals with harmful effects of environmental agents which leads to the development of the disease. AD has been described as an allergic skin disease, but today, the contribution of allergic reactions to the initiation of AD is challenged, and it is proposed that allergy is rather a consequence of AD in subjects with a concomitant underlying atopic constitution. Treatment at best achieves symptom control rather than cure; there is thus a strong need to identify alternatives for disease prevention. • AD usually starts in early childhood and can be the initial step of the so-called 'atopic march'.• The prevalence of AD is as high as 20% in children in some countries and continues to increase, affecting now not only developed countries but also lowincome countries.• AD is a complex disease, and the relationship between allergy and AD (allergy being a cause and/or an exacerbating factor of AD) is still debated.• Genetics has recently been shown to be an important risk factor for AD, and the strongest association so far with the gene encoding filaggrin has raised the recent interest in the role of skin barrier impairment in the development of AD.• Environmental factors and specifically exposure to microbes are also recognized to play a role in the development of the disease.• AD is a multifactorial disease presenting with different endophenotypes.• The prevention of AD should start as soon as possible (possibly even in utero), targeting both skin barrier, immune/allergy and environmental aspects.

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AIM:To investigate the correlation between the in vitro immune profile of probiotic strains and their ability to prevent experimental colitis in mice. METHODS:In vitro immunomodulation was assessed by measuring interleukin (IL)-12p70, IL-10, tumor necrosis factor alpha (TNFa) and interferon g (IFNg) release by human peripheral blood mononuclear cells (PBMCs) after 24 h stimulation with 13 live bacterial strains. A murine model of acute TNBS-colitis was next used to evaluate the prophylactic protective capacity of the same set of strains. RESULTS:A strain-specific in vivo protection was observed. The strains displaying an in vitro capacity to induce higher levels of the anti-inflammatory cytokine IL-10 and lower levels of the inflammatory cytokine IL-12, offered the best protection in the in vivo colitis model. In contrast, strains leading to a low IL-10/IL-12 cytokine ratio could not significantly attenuate colitis symptoms. CONCLUSION:These results show that we could predict the in vivo protective capacity of the studied lactic acid bacteria (LAB) based on the cytokine profile we established in vitro . The PBMC-based assay we used may thus serve as a useful primary indicator to narrow down the number of candidate strains to be tested in murine models for their anti-inflammatory potential.