Protocol for isolating extracellular vesicles from alveolar macrophages phagocytosing MRSA in vitro cell culture models.

Extracellular vesicles (EVs) play a crucial role in delivering bioactive cargo in infectious diseases. Here, we present a protocol for isolating EVs from alveolar macrophages (AMs) that phagocytose methicillin-resistant Staphylococcus aureus (MRSA) in vitro cell culture models. We describe steps for bacterial preparation; infection of AMs with MRSA; and isolation, purification, and characterization of EVs.

Inhibition of the neddylation E2 enzyme UBE2M in macrophages protects against E. coli-induced sepsis.

UBE2M, an essential neddylation E2 enzyme, has been implicated in the pathogenesis of various diseases, including cancers, viral infections, and obesity. However, whether UBE2M is involved in the pathogenesis of bacterial sepsis remains unclear. In an Escherichia coli (E.

Extracellular vesicles from alveolar macrophages harboring phagocytosed methicillin-resistant Staphylococcus aureus induce necroptosis.

Methicillin-resistant Staphylococcus aureus (MRSA) infection, a major cause of hospital- and community-acquired pneumonia, still has a high mortality rate. Extracellular vesicles (EVs), as crucial mediators of intercellular communication, have a significant impact on infectious diseases. However, the role of EVs from alveolar macrophages (AMs) in MRSA pneumonia remains unclear.

Integrated pan-cancer and scRNA-seq analyses identify a prognostic coagulation-related gene signature associated with tumor microenvironment in lower-grade glioma.

Cancer-associated thrombosis is a significant complication in cancer patients, leading to increased morbidity and mortality. The expression of coagulation/fibrinolysis genes, termed the "coagulome", plays a critical role in this process. Using the single-sample gene set enrichment analysis (ssGSEA), we identified seven cancer types with significantly activated coagulation pathways, focusing on lower-grade glioma (LGG) and stomach adenocarcinoma due to their predictive value for overall survival.

Extracellular vesicles derived from M2-like macrophages alleviate acute lung injury in a miR-709-mediated manner.

Acute lung injury/acute respiratory distress syndrome (ALI/ARDS) is characterised by an uncontrolled inflammatory response, and current treatment strategies have limited efficacy. Although the protective effect of M2-like macrophages (M2φ) and their extracellular vesicles (EVs) has been well-documented in other inflammatory diseases, the role of M2φ-derived EVs (M2φ-EVs) in the pathogenesis of ALI/ARDS remains poorly understood. The present study utilised a mouse model of lipopolysaccharide-induced ALI to first demonstrate a decrease in endogenous M2-like alveolar macrophage-derived EVs.