outer membrane vesicles and infected cell exosomes: new players in host immune modulation and pathogenesis.

Outer membrane vesicles (OMVs) and exosomes are essential mediators of host-pathogen interactions. Elucidating their mechanisms of action offers valuable insights into diagnosing and treating infectious diseases and cancers. However, the specific interactions of () with host cells via OMVs and exosomes in modulating host immune responses have not been thoroughly investigated.

Triggered ferroptotic albumin-tocopherol nanocarriers for treating drug-resistant breast cancer.

Ferroptosis is considered an effective method to overcome drug-resistant tumors. This study aims to use three FDA-approved biological materials, human serum albumin, D-α-tocopherol succinate, and indocyanine green, to construct a novel biocompatible nanomaterial named HTI-NPs, exploring its effect in drug-resistant breast cancer (MCF-7/ADR cells). The research results indicate that HTI-NPs can selectively inhibit the proliferation of MCF-7/ADR cells , accompanied by upregulating transferrin receptor, generating reactive oxygen species, and downregulating glutathione peroxidase 4.

Corrigendum: Exosomal CD44 transmits lymph node metastatic capacity between gastric cancer cells via YAP-CPT1A-mediated FAO reprogramming.

[This corrects the article DOI: 10.3389/fonc.2022.

Helicobacter pylori triggers inflammation and oncogenic transformation by perturbing the immune microenvironment.

The immune microenvironment plays a critical regulatory role in the pathogenesis of Helicobacter pylori (H. pylori). Understanding the mechanisms that drive the transition from chronic inflammation to cancer may provide new insights for early detection of gastric cancer.

Erratum: Circular RNA Hsa_circRNA_101996 promotes the development of Gastric Cancer via Upregulating Matrix Metalloproteinases-2/Matrix Metalloproteinases-9 through MicroRNA-143/Ten-eleven translocation-2 Pathway: Erratum.

[This corrects the article DOI: 10.7150/jca.62121.

Tumor-associated macrophages promoting PD-L1 expression in infiltrating B cells through the CXCL12/CXCR4 axis in human hepatocellular carcinoma.

The inflammation-related tumor microenvironment (TME) is one of the major driving forces of hepatocarcinogenesis. We aimed to investigate cell-to-cell communication among Hepatocellular Carcinoma (HCC) through re-analyzing HCC single-cell RNA-seq data, and to confirm such cellular interaction through and study. We found a subset of Regulatory B cells with PD-L1 expression (PD-L1 Bregs), mainly located in adjacent HCC tissues.

The characteristics and the multiple functions of integrin β1 in human cancers.

Integrins, which consist of two non-covalently linked α and β subunits, play a crucial role in cell-cell adhesion and cell-extracellular matrix (ECM) interactions. Among them, integrin β1 is the most common subunit and has emerged as a key mediator in cancer, influencing various aspects of cancer progression, including cell motility, adhesion, migration, proliferation, differentiation and chemotherapy resistance. However, given the complexity and sometimes contradictory characteristics, targeting integrin β1 for therapeutics has been a challenge.

Mesenchymal stem/stromal cells- a principal element for tumour microenvironment heterogeneity.

The heterogeneity of the tumor microenvironment (TME) is a major obstacle in cancer treatment, making most therapeutic interventions palliative rather than curative. Previous studies have suggested that the reason for the low efficacy of immunotherapy and the relapse of the original responders over time may be due to the complex network of mesenchymal stem/stromal cells (MSCs), a population of multipotent progenitor cells existing in a variety of tissues. Cancer-associated MSCs (CA-MSCs) have already been isolated from various types of tumors and are characterized by their vigorous pro-tumorigenic functions.

Hsa_circ_0073453 modulates IL-8 secretion by GC-MSCs to promote gastric cancer progression by sponging miR-146a-5p.

Gastric cancer associated mesenchymal stem cells (GC-MSCs) have been demonstrated to promote gastric cancer progression in a paracrine manner. IL-8 is highly secreted by GC-MSCs and is crucial for their oncogenic function. However, the mechanism underlying the modulation of IL-8 secretion by GC-MSCs has not been well elucidated.

Exosomal CD44 Transmits Lymph Node Metastatic Capacity Between Gastric Cancer Cells YAP-CPT1A-Mediated FAO Reprogramming.

Background: Lymph node metastasis (LNM) commonly occurs in gastric cancer (GC) and is tightly associated with poor prognosis. Exosome-mediated lymphangiogenesis has been considered an important driver of LNM. Whether exosomes directly transmit the LNM phenotype between GC cells and its mechanisms remain elusive.

Circular RNA Hsa_circRNA_101996 promotes the development of Gastric Cancer via Upregulating Matrix Metalloproteinases-2/Matrix Metalloproteinases-9 through MicroRNA-143/Ten-eleven translocation-2 Pathway.

The long-term survival rate of gastric cancer (GC) patients at advanced stages remains low worldwide. Circular RNAs (circRNAs) a newly studied type of non-coding RNA that play an important role in the pathogenesis and diagnosis of various diseases. In this research, we aimed to explore the functions of hsa_circRNA_101996 in GC cells and an animal model of GC.

Leptin induces NAFLD progression through infiltrated CD8+ T lymphocytes mediating pyroptotic-like cell death of hepatocytes and macrophages.

Background: Nonalcoholic fatty liver disease (NAFLD) is a chronic liver disease, which causes serious health problems worldwide. Hyperleptinemia and inflammatory stress are crucial in the progression of NAFLD. However, the relationship between leptin and immune cells or hepatocytes is still unclear.

RP11-323N12.5 promotes the malignancy and immunosuppression of human gastric cancer by increasing YAP1 transcription.

Background: YAP1 is a core protein of the Hippo signaling pathway and is associated with malignancy and immunosuppression. In the present study, we discovered a novel lncRNA, RP11-323N12.5, with tumor promotion and immunosuppression activities through enhancing transcription of YAP1.

IL-6 promotes PD-L1 expression in monocytes and macrophages by decreasing protein tyrosine phosphatase receptor type O expression in human hepatocellular carcinoma.

Background: We have previously discovered a relationship between the low expression of protein tyrosine phosphatase, receptor type O (PTPRO) in tumor-infiltrating T cells and immunosuppression. The aim of the present study was to investigate the relationship between decreased PTPRO and increased programmed death ligand 1 (PD-L1) in both the peripheral monocytes and tumor-infiltrating macrophages of human hepatocellular carcinoma (HCC).

Methods: The expression and correlation of all the indices were explored in monocytes and tumor-infiltrating macrophages within both human and mice HCC.

Exosomes: an important messenger in the asthma inflammatory microenvironment.

Asthma is a frequently diagnosed chronic pulmonary disease that is increasing in incidence. It is characterized by airway narrowing due to an immune response to allergens, infections, or air pollutants. Several types of cells participate in the initiation and development of asthma, including bronchial epithelial cells, smooth muscle cells, and immune cells (mast cells, T and B cells, and dendritic cells).

Interaction of transforming growth factor-β-Smads/microRNA-362-3p/CD82 mediated by M2 macrophages promotes the process of epithelial-mesenchymal transition in hepatocellular carcinoma cells.

Abnormal tumor microenvironment and the epithelial-mesenchymal transition (EMT) are important features of tumor metastasis. However, it remains unknown how signals can form complicated networks to regulate the sustainability of the EMT process. The aim of our study is to explore the possible interaction between tumor-associated macrophages and tumor cells in the EMT process mediated by microRNA (miR)-362-3p.

Inflammatory responses induced by Helicobacter pylori on the carcinogenesis of gastric epithelial GES‑1 cells.

Helicobacter pylori (HP) is a pathogenic bacterium associated with chronic gastritis, gastric ulcer and gastric cancer. In the present study, the primary carcinogenesis process of normal gastric epithelial cells (GES‑1) infected with HP was investigated. It was determined that infected gastric mucosal epithelial GES‑1 cells secreted increased interleukin‑8 (IL‑8) and IL‑23, and exhibited enhanced expression of inducible nitric oxide synthase and cyclooxygenase‑2, inducing inflammatory reactions and resulting in apoptosis.

Host derived exosomes-pathogens interactions: Potential functions of exosomes in pathogen infection.

As bilayer vesicular corpuscles secreted by different living cells, exosomes can be found in diverse body fluids and are rich in lipids, proteins, nucleic acids and other complicated components. Exosomes offer a potent mechanism for participation in intercellular transportation, such as targeted transmission of inclusions to nearby or distant cells or tissues, and assistance in intercellular information communication to change physiological functions and properties. Exosomes take part in antigen presentation for activation of immune cells and stimulate the release of inflammatory factors and the expression of immune molecules, thus modulating the immune responses of host cells.

A study on the roles of Helicobacter pylori in bile reflux gastritis and gastric cancer.

Purpose: To observe the infection rates of Helicobacter pylori (HP) in bile reflux gastritis (BRG) and gastric cancer and the clinical significance of HP eradication in BRG and gastric cancer patients complicated with HP.

Methods: 248 patients diagnosed with BRG and gastric cancer via gastroscopy were enrolled in this study. HP detection and infection rates of HP were evaluated.

PPAR Antagonizes Hypoxia-Induced Activation of Hepatic Stellate Cell through Cross Mediating PI3K/AKT and cGMP/PKG Signaling.

Background And Aims: Accumulating evidence reveals that PPAR plays a unique role in the regulation of hepatic fibrosis and hepatic stellate cells (HSCs) activation. This study was aimed at investigating the role of PPAR in hypoxia-induced hepatic fibrogenesis and its possible mechanism.

Methods: Rats used for CCl4-induced hepatic fibrosis model were exposed to hypoxia for 8 hours each day.

Curcumin inhibits gastric cancer-derived mesenchymal stem cells mediated angiogenesis by regulating NF-κB/VEGF signaling.

Cancer-derived mesenchymal stem cells (MSCs) seem to play an important role in mediating tumor angiogenesis. Recently, curcumin has been shown to display multiple therapeutic properties, including anticancer activity. In the present study, we have tried to explore the role of curcumin in regulating gastric cancer cells-derived mesenchymal stem cells (GC-MSCs) mediated angiogenesis.

Immune checkpoint molecule PD-1 acts as a novel biomarker for the pathological process of gestational diabetes mellitus.

Aim: Accumulating evidence suggested that challenge of the maternal-fetal interaction during pregnancy might cause the impairment of immunological hemostasis and lead to gestational diabetes mellitus (GDM) pathological process. Immune checkpoint molecule PD-1 is one of the critical molecule balancing immune response and immunological tolerance.

Methods: PD-1 expressions on T-cell subsets of GDM patients and control groups were measured via flow cytometric analysis and followed up.

Comparative analysis of the interaction of HSPs in dendritic cells, macrophages, RGM-1 cells infected by .

may cause chronic gastritis, even gastric cancer, however, antigen-presenting cells (APCs) are most important immune cells involved in the induction and expression of the underlying inflammatory responses to resist . To study the interaction of HSPs in dendritic cells (DCs), macrophages and RGM-1 cells infected with , HSP-27, HSP-60, HSP-70 and HSP-90 proteins were analyzed in the mucosa tissue or serum of gastritis patients caused by , and in cell supernatant of DCs, macrophages, RGM-1 infected by , or in above host cells. We found that HSP-27, HSP-60, HSP-70 and HSP-90 decreased in gastric epithelial cells, but increased significantly in DCs, macrophages.