Background: The cellular immunity of lung cancer patients is mainly the immune response of T cells, which plays an important role in tumour cell killing and immune surveillance. Transforming growth factor 1 (TGF-β1) is secreted by tumour cells that can suppress the immune response and is an important group of immune down-regulation factors. Our study aims to investigate the effect of TGF-β1 on the morphology and cellular immune function of A549 and peripheral blood mononuclear cells (PBMCs). Methods: A549 cell line was cultured, PBMCs were cultured with different concentrations of TGF-β1, and the morphology of A549 cells and PBMCs were seen. The levels of interleukin (IL)-2, IL-4, IL-6, IL-10, IFN-γ, and TNF and the numbers of CD3, CD4, CD8, CD4/CD8, and CD3 CD25 and CD4 CD25 in PBMCs were detected. Results: During co-culture of A549 with PBMCs, TGF-β1 can induced A549 showing epithelial-tomesenchymal transition, enhanced its ability of migration and infiltration. Simultaneously, TGF-β1 can depressing the growth and proliferation of PBMCs, inhibiting T-cell activation, and accelerating the PBMCs apoptosis. TGF-β1 can inhibits A549 Th1 related-cytokines, enhance Th2 related-cytokines, cause the disorder of Th1/Th2, resulting in the Th1 cellular dominate immunity decline.Conclusions: TGF-β1 may affect the secretion of related cytokines, hinder the activation of T lymphocytes, destroy the immune surveillance and killing effect of the body, and thus inhibit the cellular immunity.
In 1951, the application of titanium in orthopedics was first reported that titanium, as an inert metal, was the ideal material for fracture fixation. 1 Later, titanium was used in oral surgery because of its good biocompatibility. However, due to its low biological strength, poor wear resistance was limited to use in weight-bearing bone. With the development of materials science, titanium alloy came into being, overcoming the shortcomings of pure titanium. Because of its high strength and good biocompatibility, it is widely used in fracture fixation. In the early stage, Ti-6Al-4V and i-3AL-2.5V were applied in the field of orthopedics, but due to their toxic elements, which might lead to toxic reactions, they were gradually replaced by alloy materials such as α + β and β alloy materials. 2 Titanium and its alloy materials have stronger
Background: Considering the wide-spread misuse of antibiotics, the development of new antibacterial drugs may effectively prevent the emergence of antibiotic resistance in bacteria. The understanding of the mechanism underlying the Staphylococcus epidermidis agrC-specific binding polypeptide-mediated inhibition of S. epidermidis biofilm formation may supply ideas for the development of new antibacterial drugs. Methods: S. epidermidis cells were cultured with different concentrations (0, 100, 200, 400, 800, and 1,600 μg/mL) of agrC-specific binding polypeptide (N1) and blank (N0). Crystal violet staining was performed to test the formation of biofilms and to determine the best concentration of agrC-specific binding polypeptides, and the bacterial inhibitory concentration was also determined. At different time points (6, 12, 18, 24, and 30 h), XTT assay was used to measure bacterial viability, and the real-time quantitative polymerase chain reaction was performed to measure the expression of atlE, icaA, fbe, and icaR genes. The sulfuric acid-phenol method was used to determine polysaccharide intercellular adhesin (PIA) levels. Results:The biofilm formation ability of S. epidermidis was the lowest after treatment with 800 μg/mL agrC-specific binding polypeptide. After 6 h of culture, agrC-specific binding polypeptide upregulated the expression of atlE, icaA, fbe, and icaR and increased the bacterial viability. However, the polypeptide downregulated the expression of atlE, icaA, fbe, and icaR and inhibited S. epidermidis growth and PIA formation after 12 h of culture. Although agrC-specific binding polypeptide upregulated the expression of atlE, icaA, fbe, and icaR after 18 h, they inhibited bacterial growth and PIA formation.Conclusions: Thus, agrC-specific binding polypeptide could downregulate the expression of atlE, icaA, fbe, and icaR and inhibit PIA formation by S. epidermidis after 12 h, demonstrating its transient inhibitory effects on the biofilm formation ability of S. epidermidis. Its effective concentration was 800 μg/mL.
Background: Transforming growth factor-β1 (TGF-β1) has a wide range of biological functions. It antagonizes lymphocyte response, inhibits pro-inflammatory cytokines, and serves as a signal to turn off the immune response and inflammatory response. To study the correlation between TGF-β1 and T helper (Th)1/ Th2 cytokine levels in tree shrews, and to explore the effects of different levels of TGF-β1 on central venous catheter (CVC)-centered Staphylococcus epidermidis biofilm formation in tree shrews.Methods: Tree shrews were injected with different concentrations of TGF-β1, and venous blood was drawn after 48 h to measure the levels of Th1 and Th2 cytokines. A CVC was placed into the femoral vein, and TGF-β1 at different concentrations and PIA− (ATCC12228) and PIA+ (ATCC35984) standard strains of Staphylococcus epidermidis were injected into the tree shrews to establish a biomaterial-centered infection (BCI) model. After 72 h, the CVC was removed, and biofilm formation was detected using the API bacterial identification system, semi-quantitative biofilm formation assay, and scanning electron microscopy.Results: In the groups treated with TGF-β1 at different concentrations, the levels of Th1 cytokines interleukin-2 (IL-2), tumor necrosis factor (TNF), and interferon-γ (IFN-γ) were lower than those of normal group, while the levels of Th2 cytokines IL-6, IL-4 and IL-10 were higher than those of normal group. In the TGF-β1 groups at different concentrations, the positive rate of Staphylococcus epidermidis ATCC35984 biofilm formation was higher than that in non-TGF-β1 group, while there was no significant difference in the positive rate of Staphylococcus epidermidis ATCC12228 biofilm formation compared with that of the non-TGF-β1 group.Conclusions: TGF-β1 causes the imbalance of Th1/Th2 cytokines and Th1/Th2 shift in tree shrews, leading to Th1 cell-led decline in cellular immune function. TGF-β1 promotes PIA+ Staphylococcus epidermidis biofilm formation in the tree shrew BCI model, but it has no significant influence on PIA-Staphylococcus epidermidis biofilm formation on the surface of CVCs.
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