Background

Obesity is a major public health problem with an increasing prevalence reaching pandemic levels. The incidence and mortality for colorectal cancer is augmented in overweight and obese individuals. Previous studies demonstrated an impaired number, phenotype and functionality of natural killer (NK) cells under obese conditions. So far, the influence of obesity on NK cells in colorectal cancer tissue remained unclear. Therefore, the aim of the study was to investigate the occurrence and localization of NK cells in colorectal tumors of normal weight and diet-induced obese rats.

Methods

Wistar rats were fed a normal-fat diet (control) or a high-fat diet (HFD) to induce obesity. In half of the experimental groups azoxymethane (AOM) was injected to induce colorectal cancer. Tumors in colon and rectum were histopathologically classified in adenomas and adenocarcinomas and immunohistologically stained with the rat NK cell marker CD161. Occurrence and localization of NK cells were analyzed and quantified in the tunica mucosa and tunica submucosa of colorectal adenomas and the tunica submucosa of colorectal adenocarcinomas.

Results

NK cells are localized in the tunica mucosa and the tunica submucosa of colorectal tumors with NK cell accumulations as follicle-like aggregates especially in regions of the lamina muscularis mucosae and the lamina propria mucosae of the tunica mucosa as well as in regions of the tunica submucosa adjacent to the lamina muscularis mucosae. Although not statistically significant, the CD161 staining was clearly reduced in the tunica mucosa of colorectal tumors of rats fed a HFD compared to rats fed a control diet. Moreover, the CD161 staining in the tunica mucosa was positively correlated with the final body weight of AOM-treated rats independent of the supplied diet.

Discussion

For the first time, these results provide information about the localization and quantity of NK cells in colorectal tumor tissue of rats fed a control diet or high-fat diet. The slight reduction of NK cell number in colorectal tissue of rats fed a high-fat diet may contribute to an impaired tumor defense and the increased colorectal tumor outcome in diet-induced obese rats.

中文翻译：

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喂食对照饮食或高脂肪饮食的大鼠结直肠肿瘤组织中自然杀伤细胞的特征。

背景

肥胖是一个主要的公共卫生问题，其患病率越来越高，达到大流行水平。超重和肥胖个体的结直肠癌发病率和死亡率增加。先前的研究表明，在肥胖条件下，自然杀伤 (NK) 细胞的数量、表型和功能受损。迄今为止，肥胖对结直肠癌组织中NK细胞的影响尚不清楚。因此，本研究的目的是研究NK细胞在正常体重和饮食诱导的肥胖大鼠结直肠肿瘤中的发生和定位。

方法

给 Wistar 大鼠喂食正常脂肪饮食（对照）或高脂肪饮食（HFD）以诱导肥胖。在一半的实验组中，注射了氧化偶氮甲烷 (AOM) 以诱发结直肠癌。结肠和直肠中的肿瘤在组织病理学上分为腺瘤和腺癌，并用大鼠 NK 细胞标记物 CD161 进行免疫组织学染色。在结直肠腺瘤的黏膜和黏膜下层以及结直肠腺癌的黏膜下层中分析和量化 NK 细胞的发生和定位。

结果

NK细胞定位于鞘膜粘膜和粘膜下层结肠直肠肿瘤的与NK细胞的积累作为滤泡样尤其是在区域聚集体薄层粘膜肌层和粘膜固有层的的鞘膜粘膜以及在区域粘膜下层毗邻黏膜肌层。尽管没有统计学意义，但与喂食对照饮食的大鼠相比，喂食 HFD 的大鼠结直肠肿瘤的粘膜中CD161 染色明显减少。此外，黏膜中的 CD161 染色 与 AOM 治疗大鼠的最终体重呈正相关，而与所提供的饮食无关。

讨论

这些结果首次提供了有关喂食对照饮食或高脂肪饮食的大鼠结直肠肿瘤组织中 NK 细胞的定位和数量的信息。喂食高脂饮食的大鼠结直肠组织中 NK 细胞数量的轻微减少可能导致肿瘤防御受损和饮食诱导的肥胖大鼠结直肠肿瘤结果增加。