Sugita T, Huang C C, Abramson M
Arch Otorhinolaryngol. 1986;243(3):211-4. doi: 10.1007/BF00470624.
Since the rate of epidermal basal cell proliferation appears to be a crucial factor in the development of acquired cholesteatoma, we studied the effect of prostaglandin E2 (PGE2) and endotoxin on the growth of keratinocytes. PGE2 and endotoxins are inflammatory mediators in chronic otitis media. Various concentrations of endotoxin and PGE2 were added to keratinocytes derived from newborn rats. The synthesis of DNA was then studied by incorporation of 3H-thymidine into the keratinocytes. We found that either endotoxin or PGE2 alone inhibited DNA synthesis by keratinocytes, while endotoxin (10 micrograms/ml) and PGE2 (10 ng/ml) together stimulated DNA synthesis by keratinocytes. These findings suggest that inflammatory mediators, such as endotoxin plus PGE2, in chronic otitis media stimulate the growth of epidermal basal cells of cholesteatoma.
由于表皮基底细胞增殖速率似乎是后天性胆脂瘤发生发展的关键因素，我们研究了前列腺素E2（PGE2）和内毒素对角质形成细胞生长的影响。PGE2和内毒素是慢性中耳炎中的炎症介质。将不同浓度的内毒素和PGE2添加到新生大鼠来源的角质形成细胞中。然后通过将3H-胸腺嘧啶核苷掺入角质形成细胞来研究DNA的合成。我们发现，单独的内毒素或PGE2均可抑制角质形成细胞的DNA合成，而内毒素（10微克/毫升）和PGE2（10纳克/毫升）共同刺激角质形成细胞的DNA合成。这些发现表明，慢性中耳炎中的炎症介质，如内毒素加PGE2，可刺激胆脂瘤表皮基底细胞的生长。
