Tumor Necrosis Factor-alpha Modulation Research Articles

Electrospun PVA nanofiber mat for topical Deflazacort delivery: accentuated anti-inflammatory efficacy for wound healing

Purpose Asses the wound healing activity of Polyvinyl alcohol – Deflazacort (PVA-DEF) nanofibers mats synthesized by electrospinning technology. Methods PVA-DEF nanofiber mats were created with various PVA polymer concentrations using an electrospinning process. The morphological features and diameter of the electrospun nanofibrous mats were investigated using scanning electron microscopy (SEM). The in vitro DEF release rate from PVA electrospun nanofibrous mats was evaluated. In addition to assessing wound healing activity in vivo, histological, and immunochemical tests were conducted. Results Results revealed a uniform and smooth surface of the fiber with an average diameter of the selected fibers of 533.9 nm ± 45.83. Also, PVA electrospun nanofiber mats showed an initial burst release of more than 50% of the DEF in 1 h, and the rest of the DEF was released gradually for up to 480 min. Fickian diffusion is the main DEF release mechanism from PVA electrospun nanofiber mats. In male Wistar albino rats with 1 cm2 excision wounds, in vivo studies revealed a significant improvement in wound healing rate via modulation of tumor necrosis factor-alpha (TNF-α) and vascular endothelial growth factor (VEGF) expression. Conclusion PVA-DEF nanofiber mats can be used effectively for improving wound healing.

Extracellular inosine participates in tumor necrosis factor-alpha induced nitric oxide production in cultured Sertoli cells

Recent reports have described purinergic modulation of tumor necrosis factor-alpha (TNF-alpha) signaling in neutrophils and astrocytes. In Sertoli cells, both TNF-R1 and TNF-R2 TNF-alpha receptors are present and this cytokine modulates many functions of these cells related to the maintenance of spermatogenesis. Sertoli cells express distinct purinoreceptors and previous work has shown that these cells secrete extracellular nucleotides and their metabolites. In this work, we studied the possible role of extracellular purines in TNF-alpha signaling in cultured Sertoli cells. This cytokine increased inosine concentration from 30 min to 6 h, with no effect at 24 h. Both TNF-alpha and inosine increased nitrite accumulation and nitric oxide synthase activity. Erythro-9-(2-hydroxy-3-nonyl)adenine (EHNA), an adenosine deaminase inhibitor, abolished the TNF-alpha induced inosine increase, nitrite accumulation and nitric oxide synthase activity. These results suggest that extracellular inosine acts as intermediary in TNF-alpha stimulated nitric oxide production in cultured Sertoli cells.

The effect of oligosaccharides on the production of tumor necrosis factor-alpha by macrophage-like cell line J774/JA-4.

Stimulation and modulation of tumor necrosis factor-alpha (TNF-alpha) production during treatment of the murine macrophage-like cell line J774/JA-4 with 25 oligosaccharides were studied. Direct stimulation of TNF-alpha production by oligosaccharides was measured with a cytotoxic assay using the L929 cell line. Twelve samples showed a significantly higher production (P < or = 0.01) of TNF-alpha than the controls. Modulation of TNF-alpha production by treatment with oligosaccharides, followed by stimulation with lipopolysaccharide (LPS) from E. coli, was examined using the L929 bioassay system. In three samples TNF-alpha production increased significantly, but in four samples, production was reduced significantly (P < or = 0.01). No samples showed modulation of growth or viability of L929 cells within the first 26 hr. The present results are useful in the application of these oligosaccharides which is potentially applicable in medical and food technology.

Biologic control of the tumor necrosis factor and interleukin-1 signaling cascade

It is clear that activation of the proinflammatory cytokine cascade is both the cause and the consequence of renal injury. Recently, it has been appreciated that a rich network of signaling pathways contributes to modulation of tumor necrosis factor-alpha (TNF) and interleukin-1 (IL-1) bioactivity, both in vitro and in vivo. Insight into the checks and balances that intervene or temper endogenous cytokine effector mechanisms has arisen from an explosion of new information on the cell biology of proinflammatory cytokines. Novel mechanisms of cytokine regulation are currently being described and hold promise for therapeutic potential: soluble cytokine receptors, endogenous receptor antagonists, and anti-inflammatory cytokines such as IL-4, IL-10, and IL-13.