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Allergic contact dermatitis (ACD) is an inflammatory skin reaction whose incidence has increased and has been associated with a dietary pattern rich in saturated fats and refined sugars. Considering the increased incidence of ACD and the lack of research about the influence of a short-term high-sugar diet on dermatitis, our aim is to improve understanding of the influence of a high-sugar diet on ACD. We introduced a diet rich in sugar fifteen days before inducing contact dermatitis with oxazolone, in mice, and maintained it until the end of the experiment, which lasted three weeks in total. The dermatitis model increased cholesterol and triglycerides in the liver, and the combination of diet and dermatitis increased weight and worsened liver cholesterol measurements. Furthermore, the high-sugar diet increased the production of IL-6, IFN-γ and TNF-α in the skin, which may be involved in the increase in epithelial skin thickness observed in experimental ACD.

Emerging evidence has shown that the maternal diet influences the microbiota. Our objective was to elucidate whether synbiotic consumption during the perinatal period equally modulates offspring gut microbiota in the A/J and C57BL/6 and affects airway inflammatory cell infiltration. We administered the synbiotic to the dam throughout the whole perinatal period. To analyze the influence of gut microbiota changes on offspring health, we induced allergic airway inflammation on offspring. Twenty-four hours after the last ovalbumin challenge, pulmonary inflammation was analyzed. Perinatal synbiotic supplementation reduced eosinophilic inflammation and mucus production only in the C57BL/6 offspring. Synbiotic supplementation during the perinatal period increased the Lactobacillus genera, which could be associated with the immune regulatory effects observed in the C57BL/6 offspring. Interestingly, synbiotic supplementation increased the diversity of gut microbiota in the A/J offspring without improving airway inflammation, indicating that diversity itself was not sufficient to regulate experimental lung inflammation.