Toshiyuki Yamamoto, Ichiro Katayama, Kiyoshi Nishioka
DOI: 10.1080/000155598433403

Dermatofibroma (DF) is histologically characterized by proliferation of fibroblasts in the dermis. Multiple DFs occasionally develop in patients with autoimmune disorders under immunosuppressive therapy; however, the pathogenesis of DF is still unclear. To elucidate immunological involvement in the mechanism of the fibrosis in DF, we studied the role of interleukin-1 (IL-1), which has a number of biological functions, including proliferation and collagen production of fibroblasts, on DF-derived fibroblasts. H-thymidine incorporation was used to examine the effects of IL-1α and IL-1β in 4 cultured fibroblast strains derived from DF and 5 fibroblast strains from normal skin. Expression of mRNA of IL-1 was also analyzed by reverse transcriptase polymerase chain reaction (RT-PCR). Basal H-TdR incorporation without stimulant of DF-derived fibroblasts showed a significantly greater growth activity than normal skin-derived fibroblasts (2, 632±525 vs. 762±144 dpm, p<0.01). Both IL-1α and IL-1β showed a stronger growth-stimulatory activity on DF-derived fibroblasts in a dose-dependent manner than normal fibroblasts, and the percent H-TdR uptake of DF was 1.4-fold (IL-1α; 1,000 U/ml) and 1.3-fold (IL-1β; 1,000 U/ml) as compared with normal fibroblasts; however, the differences did not reach any significance. When increasing concentrations of IL-1 receptor antagonist (IL-1ra) were added to culture medium stimulated with IL-1α, the proliferative response of fibroblasts was significantly reduced. Expression of IL-1β mRNA was detected on both DF-derived and normal skin-derived fibroblasts, while that of IL-1α mRNA was detected only on DF-derived fibroblasts. Our results suggest that IL-1 may be involved in the fibrotic process in DF at the transcriptional level and play a role in the fibroplast proliferation in an autocrine manner.