慢性应激促进了一种人源化的鼠模型中的免疫炎症状态和头颈部癌症的生长。
Chronic stress promotes an immunologic inflammatory state and head and neck cancer growth in a humanized murine model.
机构信息
Department of Otolaryngology, Medical College of Wisconsin, Milwaukee, Wisconsin, USA.
Department of Radiation Oncology, Medical College of Wisconsin, Milwaukee, Wisconsin, USA.
出版信息
Head Neck. 2022 Jun;44(6):1324-1334. doi: 10.1002/hed.27028. Epub 2022 Mar 8.
BACKGROUND
Despite the importance of immune response and environmental stress on head and neck cancer (HNC) outcomes, no current pre-clinical stress model includes a humanized immune system.
METHODS
We investigated the effects of chronic stress induced by social isolation on tumor growth and human immune response in subcutaneous HNC tumors grown in NSG-SGM3 mice engrafted with a human immune system.
RESULTS
Tumor growth (p < 0.0001) and lung metastases (p = 0.035) were increased in socially isolated versus control animals. Chronic stress increased intra-tumoral CD4 T-cell infiltrate (p = 0.005), plasma SDF-1 (p < 0.0001) expression, and led to tumor cell dedifferentiation toward a cancer stem cell phenotype (CD44 /ALDH , p = 0.025).
CONCLUSIONS
Chronic stress induced immunophenotypic changes, increased tumor growth, and metastasis in HNC in a murine model with a humanized immune system. This model system may provide further insight into the immunologic and oncologic impact of chronic stress on patients with HNC.
背景
尽管免疫反应和环境应激对头颈癌（HNC）的结果很重要，但目前没有包括人类免疫系统的临床前应激模型。
方法
我们研究了社交隔离引起的慢性应激对 NSG-SGM3 小鼠皮下种植的具有人类免疫系统的 HNC 肿瘤生长和人类免疫反应的影响。
结果
与对照组相比，社交隔离组肿瘤生长（p<0.0001）和肺转移（p=0.035）增加。慢性应激增加了肿瘤内 CD4 T 细胞浸润（p=0.005）、血浆 SDF-1（p<0.0001）的表达，并导致肿瘤细胞向癌症干细胞表型（CD44/ALDH，p=0.025）去分化。
结论
在具有人类免疫系统的小鼠模型中，慢性应激诱导了 HNC 的免疫表型变化、肿瘤生长和转移。该模型系统可能为进一步了解慢性应激对 HNC 患者的免疫和肿瘤学影响提供依据。
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