真珠腫・上皮増殖とサイトカイン

抄録

In order to elucidate the mechanism of proliferation of cholesteatoma epidermis, the relationship with various kinds of growth factors, receptors and cytokines was studied. At the same time, programmed cell death was also studied. When expression of PCNA protein was investigated, the results suggested hyperproliferative nature of cholesteatoma epidermis. Expression of IL-1 alpha protein was observed in subepidermal cholesteatoma epidermis showing strong inflammation, indicating a correlation with the state of subepidermal inflammation. TGF alpha protein was expressed at a high frequency in cholesteatoma tissue and normal skin tissue, indicating a correlation with the degree of infiltration by subepidermal inflammatory cells. Although expression of EGF mRNA was also increased in cholesteatoma, cholesteatoma was characterized by overexpression of EGF receptor mRNA (EGF-R mRNA) in all layers of the epidermis. Increased expression of KGF mRNA was noted as a factor which affects the effects of subepidermal inflammation on epidermal proliferation. In the cholesteatoma epidermis, overexpression of KGF-R, as well as EGF-R, was observed, which suggested paracrine regulation of KGF and KGF-R. When the relationship between proliferation of cholesteatoma epidermis and programmed cell death was investigated based on tissue sections, cells undergoing apoptosis were observed in the prickled cell layer and granular layer excluding the basal cell layer, same as normal skin tissue of the external ear canal. From these findings, it is speculated that apoptosis, as well as proliferation ability of cells, is also increased in cholesteatoma epidermis to keep the balance of proliferation. In other words, proliferation of cholesteatoma epidermis is stimulated by the action of cytokines, growth factors and subepidermal inflammatory cells, while it is compensated by apoptosis, or programmed cell death.