TREM2 expression promotes liver and peritoneal M2 macrophage polarization in mice infected with Schistosoma japonicum.

Schistosomiasis is a tropical parasitic disease that damages the liver and poses a serious threat to human health. Macrophages play a key role in the development of liver granulomas and fibrosis by undergoing polarization from M1 to M2 type during schistosomiasis. Therefore, regulating macrophage polarization is important for controlling pathological changes that occur during this disease.

and analysis of TIPE1 expression in diffuse large B cell lymphoma.

TIPE1 is a gene in the TNFAIP8 family involved in immune regulation and tumorigenesis. Although previous studies demonstrated that TIPE1 might play different roles in different tumors, its expression and role in lymphoma are unclear. Here we observed TIPE1 expression in diffuse large B cell lymphoma (DLBCL).

Recombinant P40 protein of Schistosoma japonicum inhibits TREM-1 expression in RAW264.7 cells via FOXO3a.

Triggering receptor expressed on myeloid cells 1 (TREM-1) is a transmembrane glycoprotein receptor and TREM-1 expression reached the peak at 6 weeks after infection with Schistosoma japonicum and inhibited subsequently. Since TREM-1 may be involved in the macrophage polarization process, the reason for the inhibition of TREM-1 expression in chronic schistosomiasis engaged us in them. In this study, flow cytometry was used to observe TREM-1 expression in peritoneal macrophages from mice infected with Schistosoma japonicum.

Molecular markers of tuberculosis and their clinical relevance: a systematic review and meta-analysis.

Background: Since research on disease biomarkers of tuberculosis (TB) and latent tuberculosis infection (LTBI) provides hope for simple point-of-care testing, we aim to summarize and analyze the evidence for the clinical relevance of IFN-γ-inducible protein 10 (IP-10) and IFN-γ/interleukin 2 (IL-2) as diagnostic biomarkers for TB.

Methods: The search terms tuberculosis, tuberculous pleurisy, pulmonary tuberculosis, latent tuberculosis infection, biomarkers, markers, IFN-γ-inducible protein 10, IP-10, interleukin 2, and IL-2 were used to search the PubMed, Cochrane Central Register of Controlled Trials, EMBASE, Web of Science, China National Knowledge Infrastructure (CNKI), Wanfang, and Weipu databases. The retrieval time was from the establishment of the database to September 2021.

rSjP40 Inhibited the Activity of Collagen Type I Promoter Ets-1 in HSCs.

Liver fibrosis is a severe disease characterized by excessive deposition of extracellular matrix (ECM) components in the liver. Activated hepatic stellate cells (HSCs) are a major source of ECM and a key regulator of liver fibrosis. Collagen type I alpha I (COL1A1) is one of the main components of ECM and is a major component in fibrotic tissues.

Lipocalin 2 Is a Regulator During Macrophage Polarization Induced by Soluble Worm Antigens.

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 egg accumulation. The parasites' produced eggs cause the main pathology in patients.

The role of let-7b in the inhibition of hepatic stellate cell activation by rSjP40.

Background: Hepatic stellate cells (HSCs) are one of the main cell types involved in liver fibrosis induced by many factors, including schistosomes. Previous studies in our lab have shown that recombinant P40 protein from Schistosoma japonicum (rSjP40) can inhibit HSC activation in vitro. Let-7b is a member of the let-7 microRNA family and plays an inhibitory role in a variety of diseases and inflammatory conditions.

Therapeutic inhibition of miR-802 protects against obesity through AMPK-mediated regulation of hepatic lipid metabolism.

The host-parasite relationship is based on subtle interplay between parasite survival strategies and host defense mechanisms. It is well known that helminth infection, which afflicts more than one billion people globally, correlates with a decreased prevalence of obesity. Dissecting the underlying mechanisms can provide new targets for treating obesity from the host-parasite interaction perspective.

Expression of recombinant protein rSjE16 and its effects on LX-2 cells .

Objective: The activation of hepatic stellate cells (HSCs) is a key event in schistosome-induced liver fibrosis. Previous studies have shown that soluble egg antigens and the recombinant P40 protein from eggs inhibit HSC activation. In the present study, we observed the direct effect of the recombinant (r)SjE16 protein on HSCs.

Selenoprotein P inhibits cell proliferation and ROX production in HCC cells.

Selenoprotein P (SEPP1) is a kind of secretory glycoproteins with an antioxidant effect during the development of some diseases. In this study, we attempted to observe the expression of SEPP1 in livers from the patients with hepatocellular carcinoma (HCC) and explore its effect on HCC cells. All the tissues from patients with HCC were obtained from Affiliated Hospital of Nantong University.

Toxoplasma gondii excreted-secreted antigens suppress Foxp3 promoter activity via a SP1-dependent mechanism.

Toxoplasma gondii excreted-secreted antigens (ESA) could result in adverse outcomes of pregnancy including abortion, stillbirth, foetal infection or teratogenesis in mice during early stage of pregnancy. Defective generation or function of regulatory T cells (Tregs) may account for those adverse pregnancy outcomes. Forkhead box p3 (Foxp3), which is the key transcriptional factor of Tregs, modulates its development and maintains inhibitory function.

Prognostic biomarker MITD1 and its correlation with immune infiltrates in hepatocellular carcinoma (HCC).

Background: Hepatocellular carcinoma (HCC) is globally recognized as one of the most frequently occurring primary malignant liver tumors, making the identification of HCC biomarkers critically important. The protein MITD1 (Microtubule Interacting and Trafficking Domain containing 1) has been shown to interact with ESCRT-III and participates in cytokinesis, the last step in cell division. This is the first investigation into the expression of MITD1 and its prognostic value, potential biological functions and effects on the immune system in HCC patients.

rSjp40 inhibits activated hepatic stellate cells by promoting nuclear translocation of YB1 and inducing BMP-7/Smad1/5/8 pathway.

Background: Activation of hepatic stellate cells is the dominant pathogenic event during the process of liver fibrosis. Bone morphogenic protein (BMP)-7 has recently been identified as an anti-fibrotic factor and leads to phosphorylation of Smad1/5/8 in activated hepatic stellate cells. Its expression can be upregulated by the transcriptional activator, Y-Box protein-1 (YB1).

Toxoplasma gondii excreted-secreted antigens suppress Foxp3 via PI3K-AKT-mTOR signaling pathway.

Toxoplasma gondii excreted-secreted antigens (ESA) cause spontaneous abortion or fetal teratogenesis during the pregnancy in mice, especially in the early stage. Those adverse pregnancy outcomes are due to the deficit in regulatory T cells (Tregs). Forkhead box P3 (Foxp3), a critical transcription factor, modulates Tregs differentiation and its function.

rSJYB1 inhibits collagen type I protein expression in hepatic stellate cells via down-regulating activity of collagen α1 (I) promoter.

YB1 is a negative regulator in liver fibrosis. We wondered whether SJYB1, a homologous protein of YB1 from Schistosoma japonicum, has an effect on liver fibrosis in vitro. Recombinant SJYB1 (rSJYB1) protein was expressed in a bacterial system and purified by Ni-NTA His·Bind Resin.

Schistosoma japonicum soluble egg antigen inhibits TNF-α-induced IL-34 expression in hepatic stellate cells.

Hepatic fibrosis is characterized by the activation of the main collagen-producing cells of the liver, hepatic stellate cells, and is associated with inflammation. Although the involvement of numerous inflammatory cytokines has been reported, IL-34 in particular has recently been identified as a profibrotic factor in the development of hepatic fibrosis. Previous studies have found that schistosome eggs can lead to transcriptional downregulation of fibrosis-associated genes, and based on this evidence, we attempted to investigate whether or not IL-34 is regulated by soluble egg antigen (SEA).

Excreted-secreted antigens of Toxoplasma gondii inhibit Foxp3 via IL-2Rγ/JAK3/Stats pathway.

Toxoplasma gondii excreted-secreted antigens (ESA) could lead to the fetal abortion especially in the early stage of pregnancy. Deficit in regulatory T cells is a critical event in the fetal abortion. Transcription factor forkhead box p3 (Foxp3) mediates differentiation and functional roles on regulatory T cells.

rSjP40 suppresses hepatic stellate cell activation by promoting microRNA-155 expression and inhibiting STAT5 and FOXO3a expression.

Activation of hepatic stellate cells (HSCs) is the central event of the evolution of hepatic fibrosis. Schistosomiasis is one of the pathogenic factors which could induce hepatic fibrosis. Previous studies have shown that recombinant Schistosoma japonicum egg antigen P40 (rSjP40) can inhibit the activation and proliferation of HSCs.

microRNA-146a is involved in rSjP40-inhibited activation of LX-2 cells by targeting Smad4 expression.

Previous studies have demonstrated that the recombinant Schistosoma japonicum protein P40 (rSjP40) could inhibit activation of hepatic stellate cells (HSCs) through the TGF-β1/Smads signaling pathway. Since multiple microRNAs could play essential roles in HSC activation and in the process of hepatic fibrosis through targeting Smads, we attempted to seek the potential microRNAs that could be involved in rSjP40-induced inhibition of HSC activation. Using the method of quantitative real-time PCR, we found that rSjP40 could induce miR-146a expression in LX-2 cells.

rSjP40 protein promotes PPARγ expression in LX-2 cells through microRNA-27b.

miR-27b is reported to participate in the proliferation and differentiation of hepatic stellate cells (HSCs) and to regulate fat metabolism of rat HSCs by targeting retinoid X receptor α. Our previous study also indicated that the recombinant P40 protein from Schistosoma japonicum (rSjP40) inhibited the activation of HSCs. In this study, we observed the expression of miR-27b in rSjP40-treated LX-2 cells and explored its potential mechanisms.

The N-terminal pY33XL motif of CaPsy2 is critical for the function of protein phosphatase 4 in CaRad53 deactivation, DNA damage-induced filamentation and virulence in Candida albicans.

Protein phosphatase PP4 is composed of one catalytic subunit and one or two regulatory subunits and conserved in eukaryotic cells. The catalytic subunit CaPph3 forms a complex with the regulatory subunit CaPsy2, which dephosphorylates activated CaRad53 during adaptation to and recovery from MMS-mediated DNA damage. We show here that the N-terminal Y33A mutation of CaPsy2 blocks the interaction between CaPph3 and CaRad53, the deactivation of CaRad53 and the morphologic switch in recovery from genotoxic stress.

Construction of a recombinant pIRES2-EGFP-ARTS plasmid and its effect on LX-2 cells.

The inhibition of the activation of hepatic stellate cells (HSCs) and the induction of their apoptosis have been investigated as potential strategies to counteract the development and progression of liver fibrosis. Previous research has suggested that apoptosis‑related protein in the transforming growth factor‑β signaling pathway (ARTS) may serve a significant role in numerous cell types; however, little is known regarding its roles in HSCs. Total RNA was extracted from LX‑2 cells, and the human full‑length ARTS gene was obtained by reverse transcription‑polymerase chain reaction and inserted into the pIRES2‑EGFP cloning vector.

Recombinant SjP40 protein enhances p27 promoter expression in hepatic stellate cells via an E2F1-dependent mechanism.

The p27 protein plays a critical role in cell cycle arrest. Our previous studies have demonstrated that recombinant P40 protein from Schistosoma japonicum (rSjP40) could induce G1 phase arrest of cell cycle. We, therefore, attempted to observe the effect of rSjP40 on p27 promoter activity in LX-2 cells and to explore its potential mechanisms in this study.