The prevalence of many chronic noncommunicable diseases has been steadily rising over the past six decades. During this time, over 350,000 new chemical substances have been introduced to the lives of humans. In recent years, the epithelial barrier theory came to light explaining the growing prevalence and exacerbations of these diseases worldwide. It attributes their onset to a functionally impaired epithelial barrier triggered by the toxicity of the exposed substances, associated with microbial dysbiosis, immune system activation, and inflammation. Diseases encompassed by the epithelial barrier theory share common features such as an increased prevalence after the 1960s or 2000s that cannot (solely) be accounted for by the emergence of improved diagnostic methods. Other common traits include epithelial barrier defects, microbial dysbiosis with loss of commensals and colonization of opportunistic pathogens, and circulating inflammatory cells and cytokines. In addition, practically unrelated diseases that fulfill these criteria have started to emerge as multimorbidities during the last decades. Here, we provide a comprehensive overview of diseases encompassed by the epithelial barrier theory and discuss evidence and similarities for their epidemiology, genetic susceptibility, epithelial barrier dysfunction, microbial dysbiosis, and tissue inflammation.

The consumption of gluten-free products is becoming an increased alimentary habit in the general population. The scientific unfounded perception suggesting that the avoidance of gluten would improve health or that gluten could be toxic for humans are fostering medically unjustified adherences to a gluten-free diet. Currently, only patients diagnosed with celiac disease are advised to follow a strict lifelong gluten-free diet. In the same way, patients diagnosed with IgE-mediated wheat allergy must avoid exposure to wheat in any form. In that context, a third disorder, called nonceliac gluten sensitivity, characterized by distress after gluten consumption and in which neither celiac disease nor IgE-mediated allergy plays a role, has gained increased attention in the last years. Although important scientific advances have been made in the understanding of the pathologic mechanisms behind nonceliac gluten sensitivity, this disorder is still a matter of active debate in the scientific community. In the present review, the most recent advances in the immunopathology, diagnostic biomarkers and susceptibility determinants of gluten-related diseases are summarized and discussed. Furthermore, an updated overview of the new potential therapies that are currently underway for the treatment of gluten-related disorders is also provided.

Purpose of review: To describe recent developments in therapies which target the molecular mechanisms in atopic dermatitis. Recent findings: Current advances in the understanding of the molecular basis of atopic dermatitis are leading to the stratification of different atopic dermatitis phenotypes. New therapies offer the option to target-specific molecules involved in the pathophysiology of atopic dermatitis. Current new therapies under investigation aim to modulate specific inflammatory pathways associated with distinctive atopic dermatitis phenotypes, which would potentially translate into the development of personalized, targeted-specific treatments of atopic dermatitis. Summary: Despite the unmet need for well tolerated, effective, and personalized treatment of atopic dermatitis, the current standard treatments of atopic dermatitis do not focus on the individual pathogenesis of the disease. The development of targeted, phenotype-specific therapies has the potential to open a new promising era of individualized treatment of atopic dermatitis.