Inducible nitric oxide synthase regulates macrophage polarization via the MAPK signals in concanavalin A-induced hepatitis.

Introduction: Acute liver inflammatory reactions contribute to many health problems; thus, it is critical to understand the underlying pathogenic mechanisms of acute hepatitis. In this study, an experimental in vivo model of concanavalin A (ConA)-induced hepatitis was used.

Materials And Methods: C57BL/6 (wild-type, WT) or inducible nitric oxide synthase-deficient (iNOS ) mice were injected with PBS or 15 mg/kg ConA via tail vein.

Correction: Shi, H., et al. Arctigenin Attenuates Breast Cancer Progression through Decreasing GM-CSF/TSLP/STAT3/β-Catenin Signaling. 2020, , 6357.

The authors wish to make the following correction to this paper [...

Arctigenin Attenuates Breast Cancer Progression through Decreasing GM-CSF/TSLP/STAT3/β-Catenin Signaling.

Invasive breast cancer is highly regulated by tumor-derived cytokines in tumor microenvironment. The development of drugs that specifically target cytokines are promising in breast cancer treatment. In this study, we reported that arctigenin, a bioactive compound from L.

Erratum: Enrichment and characterization of cancer stem-like cells in ultra-low concentration of serum and non-adhesive culture system.

[This corrects the article on p. 1552 in vol. 10, PMID: 29887968.

Establishment of a Human Gastric Cancer Xenograft Model in Immunocompetent Mice Using the Microcarrier-6.

Gastric cancer is among the most common malignant tumors of the digestive tract. Establishing a robust and reliable animal model is the foundation for studying the pathogenesis of cancer. The present study established a mouse model of gastric carcinoma by inoculating immunocompetent mice with MKN45 cells using microcarrier.

The inhibitor of autophagy SBI-0206965 aggravates atherosclerosis through decreasing myeloid-derived suppressor cells.

Atherosclerosis (AS) is currently the leading cause of mortality worldwide, with the development of new strategies to prevent the formation and rupture of atherosclerotic plaques being a paramount area of research. Amounting evidence suggests autophagy has an important role in the pathogenesis of AS and may be a potential therapeutic target. In this study, the effect of SBI-0206965(6965), a novel inhibitor of autophagy, was tested on the development of AS in apolipoprotein E deficient (ApoE) mice.

Granulocytic myeloid-derived suppressor cells contribute to IFN-I signaling activation of B cells and disease progression through the lncRNA NEAT1-BAFF axis in systemic lupus erythematosus.

Activation of interferon (IFN)-I signaling in B cells contributes to the pathogenesis of systemic lupus erythematosus (SLE). Recent studies have shown that myeloid-derived suppressor cells (MDSCs) significantly expand in SLE patients and lupus-prone MRL/lpr mice and contribute to the pathogenesis of SLE. However, the role of SLE-derived MDSCs in regulating IFN-I signaling activation of B cells remains unknown.

Hepatoprotective effect of capsaicin against concanavalin A-induced hepatic injury via inhibiting oxidative stress and inflammation.

Immune-mediated liver injury plays a crucial role in the pathogenesis of liver diseases, which can result from viral infections, autoimmunity, alcohol intake, and drug use. Concanavalin A (Con A)-induced hepatitis is a well-characterized murine model with similar pathophysiology to that of human viral and autoimmune hepatitis. Capsaicin, a selective agonist of the transient potential vanilloid subfamily member 1 (TRPV1) receptor, exhibits anti-inflammatory effects on various causes of inflammation.

Interleukin-16 aggravates ovalbumin-induced allergic inflammation by enhancing Th2 and Th17 cytokine production in a mouse model.

Asthma is a chronic inflammatory disease that involves a variety of cytokines and cells. Interleukin-16 (IL-16) is highly expressed during allergic airway inflammation and is involved in its development. However, its specific mechanism of action remains unclear.

Transplanted adult human hepatic stem/progenitor cells prevent histogenesis of advanced hepatic fibrosis in mice induced by carbon tetrachloride.

Transplantation of adult human hepatic stem/progenitor cells (hHSPCs) has been considered as an alternative therapy, replacing donor liver transplantation to treat liver cirrhosis. This study assessed the antifibrotic effects of hHSPCs in mice with fibrosis induced by carbon tetrachloride (CCl) and examined the actions of hHSPCs on the fibrogenic activity of human hepatic stellate cells (HSCs) in a coculture system. Isolated hHSPCs expressed stem/progenitor cell phenotypic markers.

Leukadherin-1-Mediated Activation of CD11b Inhibits LPS-Induced Pro-inflammatory Response in Macrophages and Protects Mice Against Endotoxic Shock by Blocking LPS-TLR4 Interaction.

Dysregulation of macrophage has been demonstrated to contribute to aberrant immune responses and inflammatory diseases. CD11b, expressed on macrophages, plays a critical role in regulating pathogen recognition, phagocytosis, and cell survival. In the present study, we explored the effect of leukadherin-1 (LA1), an agonist of CD11b, on regulating LPS-induced pro-inflammatory response in macrophages and endotoxic shock.

Interleukin-35 in immune-related diseases: protection or destruction.

Interleukin-35 (IL-35) is a recently identified heterodimeric cytokine in the IL-12 family. It consists of an IL-12 subunit α chain (P35) and IL-27 subunit Epstein-Barr virus-induced gene 3 (EBI3) β chain. Unlike the other IL-12 family members, it signals through four unconventional receptors: IL-12Rβ2-IL-27Rα, IL-12Rβ2-IL-12Rβ2, IL-12Rβ2-GP130, and GP130-GP130.

[The activation of CD11b by leukadherin-1 alleviates endotoxic shock through promoting the aggregation and activation of myeloid-derived suppressor cells].

Objective To study the effect of CD11b agonist leukadherin-1 (LA1) on the aggregation and immunosuppressive function of myeloid-derived suppressor cells (MDSCs) and its therapeutic effect on the condition of endotoxic shock mice. Methods The percentages of MDSCs , granulocytic myeloid-derived suppressor cells(G-MDSCs)and monocytic myeloid-derived suppressor cells(M-MDSCs)in spleen were detected by flow cytometry, after C57BL/6 female mice were injected of LA1 to activate through abdominal cavity for 12 hours and 48 hours. MDSCs were induced from the femur and tibia of C57BL/6 female mice in vitro.

Ligation of CD180 contributes to endotoxic shock by regulating the accumulation and immunosuppressive activity of myeloid-derived suppressor cells through STAT3.

Myeloid-derived suppressor cells (MDSCs) play an immunosuppressive role in the pathogenesis of inflammatory diseases. CD180, a TLR-like protein, can regulate the proliferation and activation of immune cells. However, the roles of CD180 in regulating the accumulation and function of MDSCs have not been investigated.

[IL-16 aggravates dextran sulfate sodium (DSS)-induced mouse inflammatory bowel disease by promoting M1 polarization of macrophages].

Objective To investigate the role of interleukin-16 (IL-16) in the development of inflammatory bowel disease (IBD) and clarify its regulatory mechanism involved in the pathogenesis of IBD. Methods Seven-week-old wild-type C57BL/6 (WT) and IL-16 knockout (IL-16) female mice were divided into WT control group, WT dextran sulfate sodium (DSS) treatment group, IL-16 control group and IL-16 DSS treatment group. The DSS model groups were given the water with 25 g/L DSS for 7 days to establish the IBD models, while the control groups were given the normal water.

Arctigenin Ameliorates Inflammation by Regulating Accumulation and Functional Activity of MDSCs in Endotoxin Shock.

Endotoxin shock is a life-threatening response caused by a disordered immune response to an infection. MDSCs are accumulated and play a protective role in the pathogenesis of endotoxin shock. However, the regulation of MDSCs by small molecule remains unrevealed.

Enrichment and characterization of cancer stem-like cells in ultra-low concentration of serum and non-adhesive culture system.

Cancer stem cells (CSCs) play important roles in tumor initiation, metastasis, and progression. They are also mainly responsible for high treatment failure rates. Identification and characterization of CSCs are crucial for facilitating the detection, prevention, or therapy of cancer.

A paralogous pair of mammalian host restriction factors form a critical host barrier against poxvirus infection.

Host restriction factors constitute a formidable barrier for viral replication to which many viruses have evolved counter-measures. Human SAMD9, a tumor suppressor and a restriction factor for poxviruses in cell lines, is antagonized by two classes of poxvirus proteins, represented by vaccinia virus (VACV) K1 and C7. A paralog of SAMD9, SAMD9L, is also encoded by some mammals, while only one of two paralogs is retained by others.

Autophagy regulates accumulation and functional activity of granulocytic myeloid-derived suppressor cells via STAT3 signaling in endotoxin shock.

Autophagy extensively participates in immune responses and inflammatory diseases. Myeloid-derived suppressor cells (MDSCs) are derived from CD11bGr1 cells under pathological conditions and play an immunosuppressive role in the pathogenesis of cancer and inflammatory diseases. However, the role of autophagy in regulating the accumulation and activity of MDSCs remains unknown.

Vinpocetine Inhibited the CpG Oligodeoxynucleotide-induced Immune Response in Plasmacytoid Dendritic Cells.

Plasmacytoid dendritic cells (pDCs) exert dual roles in immune responses through inducing inflammation and maintaining immune tolerance. A switch of pDC phenotype from pro-inflammation to tolerance has therapeutic promise in the treatment of autoimmune diseases. Vinpocetine, a vasoactive vinca alkaloid extracted from the periwinkle plant, has recently emerged as an immunomodulatory agent.

Dendritic cell-derived nitric oxide inhibits the differentiation of effector dendritic cells.

Dendritic cells (DCs) play a pivotal role in the development of effective immune defense while avoiding detrimental inflammation and autoimmunity by regulating the balance of adaptive immunity and immune tolerance. However, the mechanisms that govern the effector and regulatory functions of DCs are incompletely understood. Here, we show that DC-derived nitric oxide (NO) controls the balance of effector and regulatory DC differentiation.

The role of CYP2A5 in liver injury and fibrosis: chemical-specific difference.

Liver injuries induced by carbon tetrachloride (CCL4) or thioacetamide (TAA) are dependent on cytochrome P450 2E1 (CYP2E1). CYP2A5 can be induced by TAA but not by CCL4. In this study, liver injury including fibrosis induced by CCL4 or TAA were investigated in wild-type (WT) mice and CYP2A5 knockout (cyp2a5 (-/-) ) mice as well as in CYP2E1 knockout (cyp2e1 (-/-) ) mice as a comparison.

[Increased expression of IL-16 in mouse skin allograft].

Objective: To detect the expression of interleukin 16 (IL-16) in skin allografts of recipient mice and the serum level of IL-16.

Methods: Two different mouse models of skin allografts were used: the isotransplant group (C57BL/6--C57BL/6, n=45) and the allotransplantation group (BALB/c--C57BL/6, n=45). The level of IL-16 in sera and skin graft homogenates was tested by ELISA at 1, 3, 5 and 7 days after transplantation and the expression of IL-16 mRNA in skin allografts was measured by reverse transcription PCR at the same time points.