Immune evasion is an important hallmark of cancer progression and tumourigenesis. Among the cancer types, cervical cancer has very high global prevalence, severely affecting female reproductive health. Its preponderance is also observed in the Indian health sector. The NLRP3 inflammasome, an intracellular complex regulates the innate immune activity and a variant gene of it has been significantly associated with cervical cancer development. We aimed to evaluate the potential role of our chitosan engineered nanoparticles (CSNP) and gallic acid conjugated chitosan (gCSNP), to modulate the NLRP3 inflammasome complex in cervical cancer cell lines to explore their novel physicochemical properties. The encapsulation of gallic acid (GA) with chitosan was performed using ion gelation method. The CSNP and gCSNP nanoparticles ranged between 155 and 181 nm as determined by zeta sizer. The conjugations were validated by FTIR and XRD analysis. In the cervical cell line model, CSNP suppressed NLRP3 inflammasome activation in contrast to gCSNP at higher doses. In contrast to gCSNP, the CSNP not only demonstrated inhibitory effect on the expression of genes coding for the NLRP3 inflammasome complex (signal 1—priming), but also decreased relative expression of gene involved in the activation of NLRP3 inflammasome complex (signal 2—activation). Conjugation of gallic acid reversed the immunosuppressor mimicking action of CSNP in cervical cancer cell line. Future research can reveal the immunomodulatory mechanism of CSNP may have its translational significance as potential treatment strategies targeting immune evasion as an important hallmark of cancer.

中文翻译：

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来自昆虫外骨骼的纳米颗粒调节宫颈癌细胞系模型中 NLRP3 炎性体复合物的激活

免疫逃避是癌症进展和肿瘤发生的重要标志。在癌症类型中，宫颈癌在全球的患病率非常高，严重影响女性生殖健康。在印度卫生部门也观察到它的优势。NLRP3 炎症小体是一种调节先天免疫活性的细胞内复合物，它的一个变异基因与宫颈癌的发展密切相关。我们旨在评估我们的壳聚糖工程纳米粒子 (CSNP) 和没食子酸偶联壳聚糖 (gCSNP) 的潜在作用，以调节宫颈癌细胞系中的 NLRP3 炎性体复合物，以探索其新的理化特性。使用离子凝胶法进行壳聚糖对没食子酸 (GA) 的包封。CSNP 和 gCSNP 纳米粒子的范围在 155 和 181 nm 之间，由 zeta sizer 确定。通过 FTIR 和 XRD 分析验证了结合。在宫颈细胞系模型中，与 gCSNP 在较高剂量下相比，CSNP 抑制了 NLRP3 炎性体激活。与 gCSNP 相比，CSNP 不仅表现出对编码 NLRP3 炎症小体复合物的基因表达的抑制作用（信号 1-引发），而且还降低了参与 NLRP3 炎症小体复合物激活的基因的相对表达（信号 2-激活） ）。没食子酸的结合逆转了 CSNP 在宫颈癌细胞系中的免疫抑制剂模拟作用。