Abstract
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.
Highlights
A kind of digenetic trematode, schistosomes are zoonotic parasites that cause human schistosomiasis
We focused on the Lipocalin 2 (LCN2) gene and explored the possible mechanisms because it upregulated in patients with S. japonicum infections
We found on the staining area and intensity revealing that LCN2 expression was increased in S. japonicum–induced inflammatory cell area of the necroticexudative granulomas (Figure 2B)
Summary
A kind of digenetic trematode, schistosomes are zoonotic parasites that cause human schistosomiasis. While several schistosoma species do exist, the primary pathogens against humans include Schistosoma mansoni (S. mansoni), Schistosoma haematobium (S. haematobium), and Schistosoma japonicum (S. japonicum) (Ross et al, 2013). Within three (3) weeks the schistosomes present inside the host body are depicted as the primary target of the immune defense. By the 8th week after infection, these reactions are at the highest point, bringing severe symptoms to the host. By the 11th to 13th week, known as the chronic infection stage, hepatic stellate cell (HSC) activation occurs, which in turn leads to the growing deposition of collagen in the liver of the host, resulting in the development of fibrosis (Pearce and MacDonald, 2002; Burke et al, 2009; Burke et al, 2011). The quality of health and life of the host is seriously impacted, resulting in acute morbidity and mortality
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