Hypo-osmotic Shock-Induced Subclinical Inflammation of Skin in a XXXX Model of Disrupted Skin Barrier Function.

@entity1 @entity32 @entity2137 @entity111 @entity2421 @entity56 @entity35
Aging disrupts skin barrier function and induces xerosis accompanied by @entity111 . In many cases, elderly @entity1 complain of @entity111 during skin hygiene care, a condition called aquagenic @entity111 of the elderly (APE). To date, the pathophysiology and mechanism of action of APE have not been elucidated. We conducted the present study to test the hypothesis that hypo-osmotic shock of epidermal cells induces @entity32 and elongation of C-fibers by @entity2137 ( @entity2137 ) as a basic mechanism of APE. The dorsal skin of HWY @entity35 , which are a model for disrupted skin barrier function, was treated with distilled water ( @entity2421 treatment [Hypo] group) or normal saline (isotonic treatment [Iso] group) by applying soaked gauze for 7 days. Untreated @entity35 were used as a control (no-treatment [NT] group). Histochemical and immunohistochemical analyses revealed inflammatory responses in the epidermis and the dermal papillary layer in the Hypo group, while no alterations were observed in the Iso or NT groups. Induction of expression and secretion of @entity2137 and elongation of C-fibers into the epidermis were found in the Hypo group. In contrast, secretion of @entity2137 was significantly lower and elongation of C-fibers was not observed in the Iso group. These results suggest that hypo-osmotic shock-induced inflammatory reactions promote @entity56 to @entity111 in skin with disrupted barrier function.
