Dermatology (Basel, Switzerland) · 1996
Reticular erythematous mucinosis syndrome: glycosaminoglycan synthesis by fibroblasts and abnormal response to interleukin-1 beta.
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Izumi T, Tajima S, Harada R, Nishikawa T
Аннотация
BACKGROUND: Reticular erythematous mucinosis (REM) syndrome is characterized by an accumulation of mucin in the dermis.
OBJECTIVE: To elucidate the mechanism of mucin deposition, the response of REM syndrome fibroblasts to various exogenous factors was studied.
METHOD: REM and control fibroblasts were treated with potent modulators including tumor necrosis factor-alpha, basic fibroblast growth factor, interferon-gamma, transforming growth factor-beta 1 and interleukin-1 alpha (IL-1 alpha) and -4.
RESULTS: IL-1 beta failed to stimulate glycosaminoglycan synthesis in REM fibroblasts whereas it stimulated glycosaminoglycan synthesis up to 6-fold in control fibroblasts. The stimulation of glycosaminoglycan was caused largely by a comparable increase in hyaluronic acid.
CONCLUSION: These results suggest that the patient fibroblasts exhibit an abnormal response to stimulation by exogenous IL-1 beta and that IL- 1 beta may be involved in the abnormal hyaluronic acid metabolism in REM syndrome.
OBJECTIVE: To elucidate the mechanism of mucin deposition, the response of REM syndrome fibroblasts to various exogenous factors was studied.
METHOD: REM and control fibroblasts were treated with potent modulators including tumor necrosis factor-alpha, basic fibroblast growth factor, interferon-gamma, transforming growth factor-beta 1 and interleukin-1 alpha (IL-1 alpha) and -4.
RESULTS: IL-1 beta failed to stimulate glycosaminoglycan synthesis in REM fibroblasts whereas it stimulated glycosaminoglycan synthesis up to 6-fold in control fibroblasts. The stimulation of glycosaminoglycan was caused largely by a comparable increase in hyaluronic acid.
CONCLUSION: These results suggest that the patient fibroblasts exhibit an abnormal response to stimulation by exogenous IL-1 beta and that IL- 1 beta may be involved in the abnormal hyaluronic acid metabolism in REM syndrome.