Caused by schistosomes, the human schistosomiasis is a tropical zoonotic parasitic disease. Pathologically, it occurs most often in the intestines and the liver, the sites of Schistosoma japonicum egg accumulation. The parasites’ produced eggs cause the main pathology in patients. Deposited parasite eggs in the liver induce the production of multiple cytokines that mediate the immune response, which in turn leads to granulomatous responses and liver fibrosis. These impact the hosts’ quality of life and health status, resulting in severe morbidity and even mortality. In this study, differentially expressed genes (DEGs) between ordinary samples and three 6- week infected mice were mined from microarray analysis based on the limma package. In total, we excavated the differential expression LCN2 was exhibited high expressions profile in GSE59276, GSE61376 demonstrated the result. Furthermore, CIBERSORT suggested detailed analysis of the immune subtype distribution pattern. In vivo experiments like real-time quantitative PCR, immunohistochemical (IHC) staining, and immunofluorescence (IF) demonstrated the expressions of LCN2 was significantly upregulated in S. japonicum–infected mice liver tissues and located in macrophages. Previous studies have shown that macrophages act as the first line of defense during schistosome infection and are an important part of liver granuloma. We used S. japonicum soluble worm antigens (SWA) to induce RAW264.7 cells to construct an in vitro inflammatory model. The current study aimed to investigate whether the NF-κB signaling network is involved in LCN2 upregulation induced by SWA and whether LCN2 can promote M1 polarization of macrophages under SWA treatment. Our research work suggests that LCN2 is significant in the development of early infection caused by S. japonicum and is of great value for further exploration. Collectively, the findings indicated that SWA promoted the expression of LCN2 and promoted M1 polarization of macrophages via the upregulation of NF-κB signaling pathway. Our findings demonstrate that NF-κB/LCN2 is necessary for migration and phagocytosis of M1 macrophages in response to SWA infection. Our study highlights the essential role of NF-κB/LCN2 in early innate immune response to infection.

由血吸虫引起的人类血吸虫病是一种热带人畜共患寄生虫病。病理学上，它最常发生在肠道和肝脏，日本血吸虫卵子堆积。寄生虫产生的卵引起患者的主要病理。在肝脏中沉积的寄生虫卵会诱导产生多种介导免疫反应的细胞因子，进而导致肉芽肿反应和肝纤维化。这些影响宿主的生活质量和健康状况，导致严重的发病率甚至死亡。在这项研究中，普通样本和三只 6 周感染小鼠之间的差异表达基因 (DEG) 是从基于 limma 包的微阵列分析中挖掘出来的。总的来说，我们挖掘了差异表达 LCN2 在 GSE59276 中表现出高表达谱，GSE61376 展示了结果。此外，CIBERSORT 建议对免疫亚型分布模式进行详细分析。体内实时定量 PCR、免疫组化 (IHC) 染色和免疫荧光 (IF) 等实验表明 LCN2 的表达在日本血吸虫- 感染小鼠肝组织并位于巨噬细胞中。既往研究表明，巨噬细胞作为血吸虫感染的第一道防线，是肝肉芽肿的重要组成部分。我们用了日本血吸虫可溶性蠕虫抗原 (SWA) 诱导 RAW264.7 细胞构建体外炎症模型。本研究旨在探讨 NF-κB 信号网络是否参与 SWA 诱导的 LCN2 上调，以及 LCN2 是否可以促进 SWA 处理下巨噬细胞的 M1 极化。我们的研究工作表明 LCN2 在由日本血吸虫对进一步探索具有重要价值。总的来说，研究结果表明 SWA 促进了 LCN2 的表达并促进了巨噬细胞的 M1 极化通过NF-κB 信号通路的上调。我们的研究结果表明，NF-κB/LCN2 是 M1 巨噬细胞响应 SWA 感染的迁移和吞噬作用所必需的。我们的研究强调了 NF-κB/LCN2 在对感染的早期先天免疫反应中的重要作用。