PMID- 7798624
OWN - NLM
STAT- MEDLINE
DCOM- 19950124
LR  - 20190723
IS  - 0022-202X (Print)
IS  - 0022-202X (Linking)
VI  - 103
IP  - 6
DP  - 1994 Dec
TI  - Occlusion lowers cytokine mRNA levels in essential fatty acid-deficient and 
      normal mouse epidermis, but not after acute barrier disruption.
PG  - 834-8
AB  - 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.
FAU - Wood, L C
AU  - Wood LC
AD  - Dermatology and Medical Services, Department of Veterans Affairs Medical Center, 
      San Francisco, CA 94121.
FAU - Elias, P M
AU  - Elias PM
FAU - Sequeira-Martin, S M
AU  - Sequeira-Martin SM
FAU - Grunfeld, C
AU  - Grunfeld C
FAU - Feingold, K R
AU  - Feingold KR
LA  - eng
GR  - AR 19098/AR/NIAMS NIH HHS/United States
GR  - AR 39448/AR/NIAMS NIH HHS/United States
GR  - AR 39639/AR/NIAMS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Invest Dermatol
JT  - The Journal of investigative dermatology
JID - 0426720
RN  - 0 (Cytokines)
RN  - 0 (Fatty Acids, Essential)
RN  - 0 (Il1rn protein, mouse)
RN  - 0 (Interleukin 1 Receptor Antagonist Protein)
RN  - 0 (Interleukin-1)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, Interleukin-1)
RN  - 0 (Sialoglycoproteins)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Animals
MH  - Cell Membrane Permeability/drug effects/physiology
MH  - Cytokines/*genetics
MH  - Fatty Acids, Essential/*deficiency
MH  - Interleukin 1 Receptor Antagonist Protein
MH  - Interleukin-1/genetics
MH  - Male
MH  - Mice
MH  - Mice, Hairless
MH  - RNA, Messenger/analysis
MH  - Receptors, Interleukin-1/antagonists & inhibitors
MH  - Sialoglycoproteins/genetics
MH  - Skin/*chemistry/*metabolism/physiopathology
MH  - Tumor Necrosis Factor-alpha/genetics
EDAT- 1994/12/01 00:00
MHDA- 1994/12/01 00:01
CRDT- 1994/12/01 00:00
PHST- 1994/12/01 00:00 [pubmed]
PHST- 1994/12/01 00:01 [medline]
PHST- 1994/12/01 00:00 [entrez]
AID - S0022-202X(94)95831-9 [pii]
AID - 10.1111/1523-1747.ep12413597 [doi]
PST - ppublish
SO  - J Invest Dermatol. 1994 Dec;103(6):834-8. doi: 10.1111/1523-1747.ep12413597.