Fruit and vegetable intakes in relation to behavioral outcomes associated with a nutrition education intervention in preschoolers.

BACKGROUND/OBJECTIVES: Although a lot of effort has been put into increasing fruit and vegetable intakes in preschool children, vegetable intake in this group is still low. This study investigated whether nutrition education focusing on fruit and vegetable intakes can affect preschoolers' fruit and vegetable intakes as well as their behavioral outcomes. SUBJECTS/METHODS: Thirty-five preschoolers (54.3% boys, n = 19) aged 4-6 years residing in Seoul underwent weekly nutrition education intervention (8 sessions) between May and July 2016. Intakes of fruits and vegetables were measured during pre and post-intervention. At snack time, fresh fruit (150 g) and vegetable (120 g) snacks were distributed to each child by teachers. The remaining portions of the snacks were weighed and recorded for each child. Behavioral outcomes were measured by applying Child behavior checklist 1.5-5 and the Diagnostic and statistical manual of mental disorders. RESULTS: During post intervention, vegetable intake increased from 36.15 ± 30.64 g to 48.01 ± 31.23 g (P = 0.010). Among the emotional and behavioral problems measured by parents, levels of total problems (P = 0.001), internalizing (P = 0.004), externalizing (P = 0.003), anxiety and depression (P = 0.001), and aggressive behavior (P = 0.005) decreased. Anxiety (P = 0.026) score, as measured by teachers, also decreased. CONCLUSIONS: Nutrition education of preschoolers regarding the intakes of fruits and vegetables had a positive effect on preschoolers' vegetable intake as well as on their emotional and behavioral outcomes. A long-term, large-scale study with a broader study design is warranted to further investigate the role of fruit and vegetable intake in cognitive development and behavior of preschoolers.

Expression of IL-22 in the Skin Causes Th2-Biased Immunity, Epidermal Barrier Dysfunction, and Pruritus via Stimulating Epithelial Th2 Cytokines and the GRP Pathway.

Increased expression of Th22 cytokine IL-22 is a characteristic finding in atopic dermatitis (AD). However, the specific role of IL-22 in the pathogenesis of AD in vivo has yet to be elucidated. Consistent with observations in human AD, IL-22 was significantly increased in the AD skin of mice after epicutaneous sensitization to house dust mite allergen. Utilizing a skin-specific inducible transgenic system, we show in the present study that expression of IL-22 in the skin of mice caused an AD-like phenotype characterized by chronic pruritic dermatitis associated with Th2-biased local and systemic immune responses, downregulation of epidermal differentiation complex genes, and enhanced dermatitis upon epicutaneous allergen exposure. IL-22 potently induced the expression of gastrin-releasing peptide (GRP), a neuropeptide pruritogen, in dermal immune cells and sensory afferents and in their skin-innervating sensory neurons. IL-22 also differentially upregulated the expression of GRP receptor (GRPR) on keratinocytes of AD skin. The number of GRP+ cells in the skin correlated with the AD severity and the intensity of pruritus. IL-22 directly upregulated the expression of epithelial-derived type 2 cytokines (thymic stromal lymphopoietin and IL-33) and GRP in primary keratinocytes. Furthermore, GRP not only strongly induced thymic stromal lymphopoietin but it also increased the expression of IL-33 and GRPR synergistically with IL-22. Importantly, we found that the expression of GRP was strikingly increased in the skin of patients with AD. These results indicate that IL-22 plays important pathogenic roles in the initiation and development of AD, in part through inducing keratinocyte production of type 2 cytokines and activation of the GRP/GRPR pathway.

An important role of α-hemolysin in extracellular vesicles on the development of atopic dermatitis induced by Staphylococcus aureus.

Skin barrier disruption and dermal inflammation are key phenotypes of atopic dermatitis (AD). Staphylococcus aureus secretes extracellular vesicles (EVs), which are involved in AD pathogenesis. Here, we evaluated the role of EVs-associated α-hemolysin derived from S. aureus in AD pathogenesis. α-hemolysin production from S. aureus was detected using western blot analyses. The cytotoxic activity of α-hemolysin on HaCaT keratinocytes was evaluated by measuring cell viability after treating cells with soluble and EVs-associated α-hemolysin. To determine the type of cell death, HaCaT keratinocytes were stained with annexin V and 7-AAD. The in vivo effects of α-hemolysin were evaluated by application of soluble and EV-associated α-hemolysin on the mouse skin. The present study showed that increased α-hemolysin was produced by S. aureus colonized on AD patients compared to healthy subjects. α-hemolysin production was also related to AD severity. In addition, EV-associated α-hemolysin was more cytotoxic to HaCaT keratinocytes than soluble α-hemolysin, and α-hemolysin-negative EVs did not induce keratinocyte death. EV-associated α-hemolysin induced necrosis, but soluble α-hemolysin induced apoptosis of keratinocytes. In vivo, skin barrier disruption and epidermal hyperplasia were induced by soluble and EV-associated α-hemolysin. However, AD-like dermal inflammation was only caused by EV-associated α-hemolysin. Moreover, neither skin barrier disruption nor AD-like skin inflammation was induced by α-hemolysin-negative EVs. Taken together, α-Hemolysin secreted from S. aureus, particularly the EV-associated form, induces both skin barrier disruption and AD-like skin inflammation, suggesting that EV-associated α-hemolysin is a novel diagnostic and therapeutic target for the control of AD.