Nanoparticles have extremely wide applications in the medical and biological fields. They are being used in biosensors, local drug delivery, diagnostics, and medical therapy. However, the potential effects of nanoparticles on target cell and tissue function, apart from cytotoxicity, are not completely understood. Thus, the aim of this study was to investigate the in vitro effects of silver nanoparticles (AgNPs) and gold nanoparticles (AuNPs) on human fibroblasts with respect to their interaction with the extracellular matrix and in cell migration. Immunofluorescence analysis revealed that treatment with AgNPs or AuNPs decreased collagen and laminin production at all the concentrations tested (0.1, 1, and 10 μg/mL). Furthermore, cytofluorometric analysis showed that treatment with AgNPs reduced the percentage of cells expressing the collagen receptor very late antigen 2, α2β1 integrin (VLA-2) and the laminin receptor very late antigen 6, α6β1 integrin (VLA-6). In contrast, AuNP treatment increased and decreased the percentages of VLA-2-positive and VLA-6-positive cells, respectively, as compared to the findings for the controls. Analysis of cytoskeletal reorganization showed that treatment with both types of nanoparticles increased the formation of stress fibres and number of cell protrusions and impaired cell polarity. Fibroblasts exposed to different concentrations of AuNPs and AgNPs showed reduced migration through transwell chambers in the functional chemotaxis assay. These results demonstrated that metal nanoparticles may influence fibroblast function by negatively modulating the deposition of extracellular matrix molecules (ECM) and altering the expression of ECM receptors, cytoskeletal reorganization, and cell migration.

Diabetes mellitus (DM) is a chronic metabolic disorder characterized by impaired glycemic regulation and persistent hyperglycemia, which drives the onset of microvascular complications such as diabetic neuropathy and nephropathy. Chronic hyperglycemia activates oxidative stress pathways and alters gut microbiota composition, both of which contribute to disease progression. In this context, probiotics have emerged as promising therapeutic agents due to their ability to modulate oxidative stress, improve glycemic control, and influence gut microbial balance. This review summarizes preclinical and clinical evidence supporting the antioxidant potential of probiotics in DM management, with a focus on underlying mechanisms. Strains from the Lactobacillus and Bifidobacterium genera are the most extensively studied and have demonstrated hypoglycemic and antioxidant effects, including the enhancement of key antioxidant enzymes and reductions in lipid peroxidation and nitrosative stress markers. Probiotics have also shown beneficial effects in DM-associated complications, particularly diabetic neuropathy and nephropathy. While clinical data are still limited, recent findings underscore oxidative stress as a critical therapeutic target influenced by probiotic interventions. Overall, current evidence supports probiotics as a complementary strategy for managing DM and its complications, highlighting the need for further well-designed clinical trials exploring diverse strains, formulations, and dosing regimens.

Understanding the pathogenesis of certain viral agents is essential for developing new treatments and obtaining a clinical cure. With the onset of the new coronavirus (SARS-CoV-2) pandemic in the beginning of 2020, a rush to conduct studies and develop drugs has led to the publication of articles that seek to address knowledge gaps and contribute to the global scientific research community. There are still no reports on the infectivity or repercussions of SARS-CoV-2 infection on the central lymphoid organ, the thymus, nor on thymocytes or thymic epithelial cells. In this brief review, we present a hypothesis about lymphopenia observed in SARS patients and the probable pathological changes that the thymus may undergo due to this new virus.

Several evidences indicate that hormones and neuropeptides function as immunomodulators. Among these, growth hormone (GH) is known to act on the thymic microenvironment, supporting its role in thymocyte differentiation. The aim of this study was to evaluate the effect of GH on human thymocytes and thymic epithelial cells (TEC) in the presence of laminin. GH increased thymocyte adhesion on BSA-coated and further on laminin-coated surfaces. The number of migrating cells in laminin-coated membrane was higher in GH-treated thymocyte group. In both results, VLA-6 expression on thymocytes was constant. Also, treatment with GH enhanced laminin production by TEC after 24 h in culture. However, VLA-6 integrin expression on TEC remained unchanged. Finally, TEC/thymocyte co-culture model demonstrated that GH elevated absolute number of double-negative (CD4−CD8−) and single-positive CD4+ and CD8+ thymocytes. A decrease in cell number was noted in double-positive (CD4+CD8+) thymocytes. The results of this study demonstrate that GH is capable of enhancing the migratory capacity of human thymocytes in the presence of laminin and promotes modulation of thymocyte subsets after co-culture with TEC.

The generation of T lymphocytes (thymopoiesis) is one of the major functions of the thymus that occurs throughout life. Thymic epithelial cells actively participate in this process. However, less attention has been paid to extracellular matrix (ECM) elements of thymus and their role in thymocyte differentiation. To clarify this topic, we selected some studies that deal with thymic ECM, its modulation, and its effects on thymopoiesis in different models. We emphasize that further studies are needed in order to deepen this knowledge and to propose new alternatives for thymic ECM functions during thymopoiesis.