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Topical and systemic immunoreaction triggered by intravesical chemotherapy in an N-butyl-N-(4-hydroxybutyl) nitorosamine induced bladder cancer mouse model

机译：N-丁基-N-（4-羟丁基）硝硝胺致膀胱癌小鼠模型中膀胱内化疗引起的局部和全身免疫反应

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Intravesical bacillus Calmette-Guerin (BCG) treatment is the most common therapy to prevent progression and recurrence of non-muscle invasive bladder cancer (NMIBC). Although the immunoreaction elicited by BCG treatment is well documented, those induced by intravesical treatment with chemotherapeutic agents are much less known. We investigated the immunological profiles caused by mitomycin C, gemcitabine, adriamycin and docetaxel in the N-butyl-N-(4-hydroxybutyl) nitrosamine (BBN)-induced orthotopic bladder cancer mouse model. Ninety mice bearing orthotopic bladder cancer induced by BBN were randomly divided into six groups and treated with chemotherapeutic agents once a week for four weeks. After last treatment, bladder and serum samples were analyzed for cell surface and immunological markers (CD4, CD8, CD56, CD204, Foxp3, and PD-L1) using immunohistochemistry staining. Serum and urine cytokine levels were evaluated by ELISA. All chemotherapeutic agents presented anti-tumor properties similar to those of BCG. These included changes in immune cells that resulted in fewer M2 macrophages and regulatory T cells around tumors. This result was compatible with those in human samples. Intravesical chemotherapy also induced systemic changes in cytokines, especially urinary interleukin (IL)-17A and granulocyte colony stimulating factor (G-CSF), as well as in the distribution of blood neutrophils, lymphocytes, and monocytes. Our findings suggest that intravesical treatment with mitomycin C and adriamycin suppresses protumoral immunity while enhancing anti-tumor immunity, possibly through the action of specific cytokines. A better understanding of the immunoreaction induced by chemotherapeutic agents can lead to improved outcomes and fewer side effects in intravesical chemotherapy against NMIBC.
机译：膀胱内卡介苗（BCG）治疗是预防非肌肉浸润性膀胱癌（NMIBC）进展和复发的最常见疗法。尽管已充分证明了BCG处理引发的免疫反应，但通过膀胱腔内用化学治疗剂诱导的免疫反应却鲜为人知。我们调查了由丝裂霉素C，吉西他滨，阿霉素和多西他赛在N-丁基-N-（4-羟丁基）亚硝胺（BBN）诱导的原位膀胱癌小鼠模型中引起的免疫学特征。将90名患有BBN诱导的原位膀胱癌的小鼠随机分为六组，每周一次用化学治疗剂治疗4周。最后一次治疗后，使用免疫组织化学染色分析膀胱和血清样品的细胞表面和免疫学标记（CD4，CD8，CD56，CD204，Foxp3和PD-L1）。通过ELISA评估血清和尿液细胞因子水平。所有化学治疗剂均表现出与BCG相似的抗肿瘤特性。其中包括免疫细胞的变化，导致肿瘤周围M2巨噬细胞和调节性T细胞减少。该结果与人类样品中的结果相容。膀胱内化疗还诱导细胞因子的系统性变化，尤其是尿白介素（IL）-17A和粒细胞集落刺激因子（G-CSF），以及血液中性粒细胞，淋巴细胞和单核细胞的分布。我们的研究结果表明，丝裂霉素C和阿霉素的膀胱内治疗可以抑制肿瘤免疫，同时增强抗肿瘤免疫，可能是通过特定细胞因子的作用。对化学治疗剂诱导的免疫反应的更好理解可以导致针对NMIBC的膀胱内化学疗法改善结局并减少副作用。

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