title: Occlusion lowers cytokine mRNA levels in essential fatty acid-deficient and normal mouse epidermis, but not after acute barrier disruption.
abstract: Acute disruption of the permeability barrier by either tape stripping or acetone treatment and chronic disruption by feeding an essential fatty acid-deficient diet increase the mRNA levels of tumor necrosis factor-alpha (TNF alpha), interleukin (IL)-1 alpha, IL-1 beta, IL-1ra, and granulocyte/macrophage-colony-stimulating factor in murine epidermis. Furthermore, epidermal TNF alpha protein levels also are stimulated by barrier disruption. To understand the relation of epidermal cytokine production to barrier function, we studied the effect of the application of a water vapor-impermeable membrane on epidermal cytokine production both in normal epidermis and after barrier disruption. Latex occlusion of essential fatty acid-deficient mice for 24-48 h lowered the mRNA levels of epidermal TNF alpha, IL-1 alpha, and IL-1ra to nearly control values, but not the levels of IL-1 beta mRNA. Occlusion of normal mice for 8, 24, and 48 h did not alter the levels of epidermal mRNAs encoding TNF alpha, IL-1 beta, or IL-1ra. Yet mRNA levels of IL-1 alpha, the major constitutively produced epidermal cytokine, were reduced by 40% after 24 h and by 80% after 48 h of occlusion of normal mouse epidermis. In contrast, latex occlusion of mice immediately after acute barrier disruption by either tape stripping or acetone treatment blocked neither the stimulation of epidermal mRNAs for TNF alpha, IL-1 alpha, IL-1 beta, or IL-1ra, nor the increase in epidermal TNF alpha protein. Taken together, these results suggest that barrier status regulates the production of specific cytokines in essential fatty acid-deficient and normal mouse epidermis. However, the signals that regulate epidermal cytokine production in response to acute barrier disruption do not appear to be influenced by occlusion.
authors.affiliation: Dermatology and Medical Services, Department of Veterans Affairs Medical Center, San Francisco, CA 94121.
authors.forename: L C
authors.initials: LC
authors.lastname: Wood
authors.forename: P M
authors.initials: PM
authors.lastname: Elias
authors.forename: S M
authors.initials: SM
authors.lastname: Sequeira-Martin
authors.forename: C
authors.initials: C
authors.lastname: Grunfeld
authors.forename: K R
authors.initials: KR
authors.lastname: Feingold
mesh_terms: D000818:Animals; D002463:Cell Membrane Permeability / Q000187:drug effects / Q000502:physiology; D016207:Cytokines / Q000235:genetics*; D005228:Fatty Acids, Essential / Q000172:deficiency*; D053590:Interleukin 1 Receptor Antagonist Protein; D007375:Interleukin-1 / Q000235:genetics; D008297:Male; D051379:Mice; D008812:Mice, Hairless; D012333:RNA, Messenger / Q000032:analysis; D017472:Receptors, Interleukin-1 / Q000037:antagonists & inhibitors; D012795:Sialoglycoproteins / Q000235:genetics; D012867:Skin / Q000737:chemistry* / Q000378:metabolism* / Q000503:physiopathology; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics
chemical_list: D016207:Cytokines; D005228:Fatty Acids, Essential; C507764:Il1rn protein, mouse; D053590:Interleukin 1 Receptor Antagonist Protein; D007375:Interleukin-1; D012333:RNA, Messenger; D017472:Receptors, Interleukin-1; D012795:Sialoglycoproteins; D014409:Tumor Necrosis Factor-alpha