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.
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