Development of a colloidal gold-based immunochromatographic assay for rapid detection of nasal mucosal secretory IgA against SARS-CoV-2.

Introduction: Infection with SARS-CoV-2 begins in the upper respiratory tract and can trigger the production of mucosal spike-specific secretory IgA (sIgA), which provides protection against reinfection. It has been recognized that individuals with high level of nasal spike-specific IgA have a lower risk of reinfection. However, mucosal spike-specific sIgA wanes over time, and different individuals may have various level of spike-specific sIgA and descending kinetics, leading to individual differences in susceptibility to reinfection. A method for detecting spike-specific sIgA in the nasal passage would be valuable for predicting the risk of reinfection so that people at risk can have better preparedness. Methods: In this study, we describe the development of a colloidal gold-based immunochromatographic (ICT) strip for detecting SARS-CoV-2 Omicron spike-specific sIgA in nasal mucosal lining fluids (NMLFs). Results: The ICT strip was designed to detect 0.125 µg or more spike-specific sIgA in 80 µL of NMLFs collected using a nasal swab. Purified nasal sIgA samples from individuals who recently recovered from an Omicron BA.5 infection were used to demonstrate that this ICT strip can specifically detect spike-specific sIgA. The signal levels positively correlated with neutralizing activities against XBB. Subsequent analysis revealed that people with low or undetectable levels of spike-specific sIgA in the nasal passage were more susceptible to SARS-CoV-2 reinfection. Conclusions: This nasal spike-specific sIgA ICT strip provides a non-invasive, rapid, and convenient method to assess the risk of reinfection for achieving precision preparedness.

Ginkgolide B inhibits the malignant biological behaviors of gastric cancer HGC-27 cells by blocking the PI3K/Akt/mTOR signaling pathway / 中国肿瘤生物治疗杂志

@#[摘 要] 目的：探讨银杏内酯B（GKB）是否通过阻抑PI3K/Akt/mTOR信号通路抑制胃癌HGC-27细胞的增殖、凋亡、迁移及侵袭。方法：将HGC-27细胞分为对照、GKB低剂量（100 mg/L）、GKB高剂量（200 mg/L）、GKB高剂量（200 mg/L）+740Y-P（PI3K激活剂）、Ly294002（PI3K抑制剂）组。采用MTT、Edu、FCM、Transwell实验分别检测各组细胞的增殖、凋亡、迁移和侵袭能力，qPCR和WB法分别检测各组细胞中PI3K mRNA、Akt mRNA、mTOR mRNA和Ki-67、caspase-3、p-PI3K/PI3K、p-Akt/Akt、p-mTOR/mTOR蛋白的表达。构建胃癌HGC-27细胞裸鼠移植瘤模型，观察GKB对移植瘤生长的影响，WB法检测移植瘤组织中Ki-67、caspase-3、p-PI3K/PI3K、p-Akt/Akt、p-mTOR/mTOR蛋白的表达。结果：体外实验结果表明，与对照组相比，GKB低剂量组、GKB高剂量组、Ly294002组HGC-27细胞的增殖活力及细胞增殖率、迁移和侵袭细胞数，PI3K、Akt、mTOR mRNA表达，以及Ki-67、p-PI3K/PI3K、p-Akt/Akt、p-mTOR/mTOR蛋白表达均显著降低（均P<0.05）；细胞凋亡率、caspase-3蛋白表达均显著升高（均P<0.05）；740Y-P可部分逆转GKB对HGC-27细胞的抑制作用（均P<0.05）。荷瘤裸鼠实验结果显示，GKB可显著抑制HGC-27细胞裸鼠移植瘤的生长（P<0.05），且可下调PI3K/Akt/mTOR通路相关蛋白的表达。结论：GKB可通过阻抑PI3K/Akt/mTOR信号通路而抑制胃癌HGC-27细胞增殖、迁移与侵袭并促进其凋亡。