title: Altered permeability and disordered cutaneous immunoregulatory function in mice with acute barrier disruption.
abstract: In vivo and in vitro T-cell-activating ability of murine epidermal cells (EC) was investigated in acutely barrier-disrupted skin by extraction of epidermal lipids with acetone or removal of corneocytes by tape stripping. Contact sensitivity (CS) to 2,4-dinitrofluorobenzene (DNFB) and picryl chloride (PCl) and contact photosensitivity (CPS) to tetrachlorosalicylanilide (TCSA) were significantly augmented when challenged or sensitized at sites treated with acetone 24 h before, compared with the intact skin. CS to DNFB was also enhanced by tape stripping, but not by water rubbing, suggesting that physical stress or a toxic effect of acetone was not responsible for the augmentation. Semi-quantification of TCSA-EC photoadducts showed markedly increased permeability of hapten in the epidermis 24 h after acetone treatment. Bioactive IL-1alpha was more pronounced in barrier-disrupted than in intact skin. Lymph node T cells from PCl-sensitized mice proliferated significantly more in a hapten-specific and co-stimulatory molecule-dependent manner in response to trinitrophenylated (TNP) EC from acetone-treated skin than to those from untreated skin. Immunofluorescence staining of epidermal sheets and flow cytometric analysis of dispersed EC showed that subpopulations of Langerhans cells (LC) in acetone-rubbed or tape-stripped skin expressed major histocompatibility complex class II CD54 and CD86 molecules at levels higher than the rest of LC and LC from water-treated or untreated epidermis. Therefore, not only increased permeability of hapten through the epidermis but also altered immune functions of EC potentiate T-cell activation in acute barrier disruption. Such augmentation of immune reactivity may be critical to elimination of environmental noxious agents that penetrate easily into the barrier-disrupted epidermis.
authors.affiliation: Department of Dermatology, Hamamatsu University School of Medicine, Handa-cho, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Nishijima
authors.forename: Y
authors.initials: Y
authors.lastname: Tokura
authors.forename: G
authors.initials: G
authors.lastname: Imokawa
authors.forename: N
authors.initials: N
authors.lastname: Seo
authors.forename: F
authors.initials: F
authors.lastname: Furukawa
authors.forename: M
authors.initials: M
authors.lastname: Takigawa
mesh_terms: D000096:Acetone / Q000494:pharmacology; D000818:Animals; D017951:Antigen Presentation / Q000502:physiology; D015703:Antigens, CD / Q000096:biosynthesis; D051940:B7-2 Antigen; D002463:Cell Membrane Permeability / Q000187:drug effects / Q000502:physiology; D003877:Dermatitis, Contact / Q000276:immunology* / Q000503:physiopathology*; D004139:Dinitrofluorobenzene / Q000494:pharmacology; D000949:Histocompatibility Antigens Class II / Q000096:biosynthesis; D018799:Intercellular Adhesion Molecule-1 / Q000096:biosynthesis; D007375:Interleukin-1 / Q000502:physiology; D007801:Langerhans Cells / Q000276:immunology; D008213:Lymphocyte Activation; D008297:Male; D008562:Membrane Glycoproteins / Q000096:biosynthesis; D051379:Mice; D008807:Mice, Inbred BALB C; D012867:Skin / Q000166:cytology* / Q000187:drug effects; D013601:T-Lymphocytes / Q000276:immunology; D014870:Water Loss, Insensible / Q000187:drug effects
chemical_list: D015703:Antigens, CD; D051940:B7-2 Antigen; C497965:Cd86 protein, mouse; D000949:Histocompatibility Antigens Class II; D007375:Interleukin-1; D008562:Membrane Glycoproteins; D018799:Intercellular Adhesion Molecule-1; D000096:Acetone; D004139:Dinitrofluorobenzene