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首页> 外文期刊>Cytokine >Intestinal inflammatory cytokine response in relation to tumorigenesis in the Apc Min/+ mouse
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Intestinal inflammatory cytokine response in relation to tumorigenesis in the Apc Min/+ mouse

机译：与Apc Min / +小鼠肿瘤发生有关的肠道炎症细胞因子反应

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The etiology of colon cancer is a complex phenomenon that involves both genetic and environmental factors. However, only about 20% have a familial basis with the largest fraction being attributed to environmental causes that can lead to chronic inflammation. While the link between inflammation and colon cancer is well established, the temporal sequence of the inflammatory response in relation to tumorigenesis has not been characterized. We examined the timing and magnitude of the intestinal inflammatory cytokine response in relation to tumorigenesis in the . Apc Min/+ mouse. . Apc Min/+ mice and wildtype mice were sacrificed at one of 4 time-points: 8, 12, 16, and 20. weeks of age. Intestinal tissue was analyzed for polyp burden (sections 1, 4 and 5) and mRNA expression and protein concentration of MCP-1, IL-1β, IL-6 and TNF-α (sections 2 and 3). The results show that polyp burden was increased at 12, 16 and 20. weeks compared to 8. weeks (P. 0.05). Gene expression (mRNA) of MCP-1, IL-1β, IL-6 and TNF-α was increased in sections 2 and 3 starting at week 12 (P. 0.05), with further increases in MCP-1, IL-1β and IL-6 at 16. weeks (P. 0.05). Protein concentration for these cytokines followed a similar pattern in section 3. Similarly, circulating MCP-1 was increased at 12. weeks (P. 0.05) and then again at 20. weeks (P. 0.05). In general, overall polyp number and abundance of large polyps were significantly correlated with the inflammatory cytokine response providing further support for a relationship between polyp progression and these markers. These data confirm the association between intestinal cytokines and tumorigenesis in the . Apc Min/+ mouse and provide new information on the timing and magnitude of this response in relation to polyp development. These findings may lead to the development of inflammatory mediators as important biomarkers for colon cancer progression. Further, these data may be relevant in the design of future investigations of therapeutic interventions to effectively target inflammatory processes in rodent models.
机译：结肠癌的病因学是一个复杂的现象，涉及遗传和环境因素。但是，只有约20％的人具有家族背景，其中最大的一部分是可导致慢性炎症的环境原因。尽管炎症和结肠癌之间的联系已经很好地建立了，但是与肿瘤发生有关的炎症反应的时间序列尚未得到表征。我们检查的时间和大小的肠道炎症细胞因子反应与肿瘤的发生。 Apc Min / +鼠标。 。在4个时间点之一：8、12、16和20周龄处死Apc Min / +小鼠和野生型小鼠。分析肠组织的息肉负担（第1、4和5节）以及MCP-1，IL-1β，IL-6和TNF-α的mRNA表达和蛋白质浓度（第2和3节）。结果显示，与8周相比，息肉负担在12周，16周和20周增加了（P <0.05）。从第12周开始，第2部分和第3部分中MCP-1，IL-1β，IL-6和TNF-α的基因表达（mRNA）增加（P <.0.05），而MCP-1，IL-1β进一步增加16周时IL-6和IL-6（P ＜0.05）。这些细胞因子的蛋白质浓度在第3节中遵循类似的模式。类似地，循环MCP-1在第12周时增加（P <.0.05），然后在第20周时再次增加（P <.0.05）。通常，总息肉数目和大息肉的丰度与炎性细胞因子反应显着相关，为息肉进展与这些标志物之间的关系提供了进一步的支持。这些数据证实了肠道细胞因子与肝癌发生的关系。 Apc Min / +鼠标，并提供有关息肉发育相关反应的时机和强度的新信息。这些发现可能导致炎症介质的发展成为结肠癌进展的重要生物标志物。此外，这些数据可能与将来设计治疗干预措施以有效地靶向啮齿动物模型中的炎症过程有关。

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