Archivum Immunologiae et Therapiae Experimentalis最新文献

The rapid development of nanotechnology has led to the use of silver nanoparticles (Ag-NPs) in various biomedical fields. However, the effect of Ag-NPs on human mesenchymal stem cells (hMSCs) is not fully understood. Moreover, too frequent an exposure to products containing nanosilver in sublethal amounts raises widespread concerns that it will lead to the development of silver-resistant microorganisms. Therefore, this study aimed to evaluate the mechanism of action of Ag-NPs on hMSCs by analyzing the cellular uptake of Ag-NPs by the cells and its effect on their viability and to assess antimicrobial activity of Ag-NPs against emerging bacterial strains, including multidrug-resistant pathogens. For metabolic activity and viability evaluation, hMSCs were incubated with different concentrations of Ag-NPs (14 μg/mL, 7 μg/mL, and 3.5 μg/mL) for 10 min., 1 h and 24 h and subsequently analyzed for their viability by live-dead staining and metabolic activity by the MTS assay. The effect of Ag-NPs on bacterial pathogens was studied by determining their minimum inhibitory concentration (MIC) and minimum bactericidal concentration (MBC). In conclusion, it was observed that exposure of hMSCs to Ag-NPs of size <10 nm has no cytotoxic effect on the metabolic activity of the cells at the concentration of 3.5 μg/mL, with minimal cytotoxic effect being observed at the concentration of 14 μg/mL after 24 h of incubation. Our findings also confirmed that Ag-NPs at the concentration of 4 μg/mL are effective broad-spectrum bactericidal agents, regardless of the antibiotic-resistance mechanism present in bacteria.

The immune system is regulated by a complex set of genetic, molecular, and cellular interactions. Rapid advances in the study of immunity and its network of interactions have been boosted by a spectrum of "omics" technologies that have generated huge amounts of data that have reached the status of big data (BD). With recent developments in artificial intelligence (AI), theoretical and clinical breakthroughs could emerge. Analyses of large data sets with AI tools will allow the formulation of new testable hypotheses open new research avenues and provide innovative strategies for regulating immunity and treating immunological diseases. This includes diagnosis and identification of rare diseases, prevention and treatment of autoimmune diseases, allergic disorders, infectious diseases, metabolomic disorders, cancer, and organ transplantation. However, ethical and regulatory challenges remain as to how these studies will be used to advance our understanding of basic immunology and how immunity might be regulated in health and disease. This will be particularly important for entities in which the complexity of interactions occurring at the same time and multiple cellular pathways have eluded conventional approaches to understanding and treatment. The analyses of BD by AI are likely to be complicated as both positive and negative outcomes of regulating immunity may have important ethical ramifications that need to be considered. We suggest there is an immediate need to develop guidelines as to how the analyses of immunological BD by AI tools should guide immune-based interventions to treat various diseases, prevent infections, and maintain health within an ethical framework.

Impaired autophagy, due to the dysfunction of lysosomal organelles, contributes to maladaptive responses by pathways central to the immune system. Deciphering the immune-inflammatory ecosystem is essential, but remains a major challenge in terms of understanding the mechanisms responsible for autoimmune diseases. Accumulating evidence implicates a role that is played by a dysfunctional autophagy-lysosomal pathway (ALP) and an immune niche in psoriasis (Ps), one of the most common chronic skin diseases, characterized by the co-existence of autoimmune and autoinflammatory responses. The dysregulated autophagy associated with the defective lysosomal system is only one aspect of Ps pathogenesis. It probably cannot fully explain the pathomechanism involved in Ps, but it is likely important and should be seriously considered in Ps research. This review provides a recent update on discoveries in the field. Also, it sheds light on how the dysregulation of intracellular pathways, coming from modulated autophagy and endolysosomal trafficking, characteristic of key players of the disease, i.e., skin-resident cells, as well as circulating immune cells, may be responsible for immune impairment and the development of Ps.

Most gastric cancers (GC) are thought to be caused by Helicobacter pylori (H. pylori) infections. However, there is mounting evidence that GC patients with positive H. pylori status have improved prognoses. The H. pylori-induced cellular immune reaction may inhibit cancer. In this study, BALB/c mice were immunized using recombinant plasmids that encode the ureF gene of H. pylori. Purified functional splenic CD3⁺ T lymphocytes are used to study the anticancer effects in vitro and in vivo. The immunological state of GC patients with ongoing H. pylori infection is mimicked by the H. pylori DNA vaccines, which cause a change in the reaction from Th1 to Th2. Human GC cells grow more slowly when stimulated CD3⁺ T lymphocytes are used as adoptive infusions because they reduce GC xenograft development in vivo. The more excellent ratios of infiltrating CD8⁺/CD4⁺ T cells, the decreased invasion of regulatory FOXP3⁺ Treg lymphocytes, and the increased apoptosis brought on by Caspase9/Caspase-3 overexpression and Survivin downregulation may all contribute to the consequences. Our findings suggest that in people with advanced GC, H. pylori pIRES2-DsRed-Express-ureF DNA vaccines may have immunotherapeutic utility.