Induction of interleukin-1 and tumor necrosis factor by 12-O-tetradecanoylphorbol-13-acetate in phorbol ester-sensitive (SENCAR) and resistant (B6C3F1) mice.
Induction of interleukin-1 and tumor necrosis factor by 12-O-tetradecanoylphorbol-13-acetate in phorbol ester-sensitive (SENCAR) and resistant (B6C3F1) mice.
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在佛波酯敏感 (SENCAR) 和耐药 (B6C3F1) 小鼠中，12-O-十四烷酰佛波醇-13-乙酸酯诱导白介素-1 和肿瘤坏死因子。
DOI：
10.1093/carcin/10.6.1107
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发表时间：
1989
期刊：
影响因子：
4.7
通讯作者：
Yim,GK
中科院分区：
文献类型：
--
作者：
Updyke,LW;Yoon,HL;Chuthaputti,A;Pfeifer,RW;Yim,GK
12-O-十四烷酰佛波醇-13-乙酸酯 (TPA) 是已知最有效的皮肤肿瘤促进剂，局部应用后会在小鼠皮肤中引起显着的炎症反应。据推测，浸润性炎症细胞通过产生活性氧中间体（ROI）而导致表皮细胞的遗传损伤，从而促进肿瘤的发展。白细胞介素-1 (IL-1) 和肿瘤坏死因子 (TNF)，小分子。已知巨噬细胞 (MP) 产生的 wt 细胞因子在炎症过程中具有重要作用。每周两次局部应用 8 μg TPA 后，在佛波酯敏感 (SENCAR) 和耐药 (B6C3F1) 小鼠的脾 MP 培养上清液中测定脂多糖 (LPS) 触发的 IL-1 和 TNF 释放。本文报告的结果表明，局部应用 TPA 引发的 SENCAR 和 B6C3F1 小鼠的脾脏 MP，以定量相似的方式产生 IL-1 和 TNF；此外，对照（初始或丙酮给药）SENCAR 和 B6C3F1 小鼠的脾 MP 响应体外 LPS 触发而释放的 IL-1 和 TNF 没有显着差异。因此，活化的 MP 产生和释放这些细胞因子与报道的对 TPA 诱导的炎症和/或肿瘤促进的菌株依赖性敏感性无关。
12-O-tetradecanoylphorbol-13-acetate (TPA), the most potent skin tumor promoter known, evokes significant inflammatory responses in mouse skin after topical application. Infiltrating inflammatory cells have been hypothesized to contribute to genetic damage in epidermal cells through the generation of reactive oxygen intermediates (ROIs), thus facilitating the development of tumors. Interleukin-1 (IL-1) and tumor necrosis factor (TNF), small mol. wt cytokines produced by macrophages (MPs), are known to have important roles in the inflammatory process. Lipopolysaccharide (LPS)-triggered release of IL-1 and TNF was determined in culture supernatants of splenic MPs from phorbol ester-sensitive (SENCAR) and resistant (B6C3F1) mice following topical application of 8 μg of TPA twice in one week. The findings reported herein indicated that topical application of TPA primed splenic MPs from both SENCAR and B6C3F1 mice in a quantitatively similar manner for the production of IL-1 and TNF; in addition, the release of IL-1 and TNF by splenic MPs from control (naive or acetone-dosed) SENCAR and B6C3F1 mice in response to LPS-triggeringin vitrowas not significantly different. Therefore, the production and release of these cytokines by activated MPs does not correlate with the reported strain-dependent susceptibilities to TPA-induced inflammation and/or tumor promotion.