scholarly journals Additive Manufacturing of Astragaloside-Containing Polyurethane Nerve Conduits Influenced Schwann Cell Inflammation and Regeneration

Processes ◽  
2021 ◽  
Vol 9 (2) ◽  
pp. 353
Author(s):  
Yueh-Sheng Chen ◽  
Shih-Sheng Chang ◽  
Hooi Yee Ng ◽  
Yu-Xuan Huang ◽  
Chien-Chang Chen ◽  
...  
Keyword(s):  
Nervous System ◽  
Cellular Proliferation ◽  
Neural Regeneration ◽  
Nerve Grafting ◽  
Necrosis Factor Alpha ◽  
Digital Light Processing ◽  
Nerve Conduits ◽  
Tnf Α ◽  
The Central Nervous System ◽  
Factor Alpha

The peripheral nervous system is the bridge of communication between the central nervous system and other body systems. Autologous nerve grafting is the mainstream method for repair of nerve lesions greater than 20 mm. However, there are several disadvantages and limitations of autologous nerve grafting, thus prompting the need for fabrication of nerve conduits for clinical use. In this study, we successfully fabricated astragaloside (Ast)-containing polyurethane (PU) nerve guidance conduits via digital light processing, and it was noted that the addition of Ast improved the hydrophilicity of traditional PU conduits by at least 23%. The improved hydrophilicity not only led to enhanced cellular proliferation of rat Schwann cells, we also noted that levels of inflammatory markers tumor necrosis factor-alpha (TNF-α) and cyclooxygenase-2 (COX-2) significantly decreased with increasing concentrations of Ast. Furthermore, the levels of neural regeneration markers were significantly enhanced with the addition of Ast. This study demonstrated that Ast-containing PU nerve conduits can be potentially used as an alternative solution to regenerate peripheral nerve injuries.

scholarly journals Central Nervous System Demyelination Related to Tumour Necrosis Factor Alpha Inhibitor

2022 ◽  
Vol 8 (1) ◽  
pp. 205521732110707
Author(s):  
Shin Yee Chey ◽  
Allan G. Kermode
Keyword(s):  
Multiple Sclerosis ◽  
Central Nervous System ◽  
Nervous System ◽  
Tumour Necrosis ◽  
Tumour Necrosis Factor Alpha ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Necrosis Factor

Background An association between tumour necrosis factor alpha (TNF-α) inhibitors exposure and central nervous system (CNS) demyelinating disorders has been postulated but is poorly understood. Objectives Describe the clinical spectrum and progress of a cohort of patients who developed demyelinating disorder following exposure to TNF-α inhibitor. Methods Retrospective chart review of patients who presented to a single neurologist in Western Australia between May 2003 and July 2020. Results 7 patients (6 females and 1 male) were identified. Mean age was 49.1 years. Mean follow-up time was 2.9 years. Mean interval between commencement of TNF-α inhibitor and onset of demyelinating event was 3 years. The spectrum of demyelinating events included transverse myelitis ( N = 3), acute brainstem syndrome ( N = 1) and optic neuritis ( N = 1). 2 patients had an atypical presentation but had MRI findings which unequivocally showed demyelinating changes. 2 patients had a monophasic event while the other 5 patients were diagnosed to have multiple sclerosis. All symptomatic patients with multiple sclerosis were started on disease modifying therapy and remained relapse free during follow-up. Conclusion Exposure to TNF-α inhibitor appears to increase the risk of demyelinating event. Whether TNFα inhibition directly results in CNS demyelination or trigger demyelination in susceptible individuals requires further research.

scholarly journals Intracerebral injection of proinflammatory cytokines or leukocyte chemotaxins induces minimal myelomonocytic cell recruitment to the parenchyma of the central nervous system.

1992 ◽  
Vol 176 (1) ◽  
pp. 255-259 ◽  
Author(s):  
P B Andersson ◽  
V H Perry ◽  
S Gordon
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Leukocyte Adhesion ◽  
Platelet Activating Factor ◽  
Intracerebral Injection ◽  
Necrosis Factor Alpha ◽  
Cell Recruitment ◽  
The Central Nervous System ◽  
Factor Alpha ◽  
Necrosis Factor

Neither excitotoxic neurodegeneration nor lipopolysaccharide induces an acute myelomonocytic exudate in the murine central nervous system (CNS) parenchyma (Andersson, P.-B., V. H. Perry, and S. Gordon. 1991. Neuroscience, 42:201; Andersson, P.-B., V. H. Perry, and S. Gordon. 1992. Neuroscience 48:169). In this study formyl-methionyl-leucyl-phenylalanine, platelet-activating factor, interleukin 8 (IL-8), IL-1, or tumor necrosis factor alpha were injected into the hippocampus to assess whether these leukocyte chemotaxins and known mediators of recruitment could bypass this block. They induced morphologic activation of microglia and widespread leukocyte margination but little or no cell exudation into the CNS parenchyma. By contrast, there was acute myelomonocytic cell recruitment to the choroid plexus, meninges, and ventricular system, comparable to that in the skin after subcutaneous injection. The normal CNS parenchyma appears to be a tissue unique in its resistance to leukocyte diapedesis, which is shown here to be at a step beyond chemotactic cytokine secretion or induction of leukocyte adhesion to cerebral endothelium.

scholarly journals TNF-α Modulates P-Glycoprotein Expression and Contributes to Cellular Proliferation via Extracellular Vesicles

Cells ◽  
2019 ◽  
Vol 8 (5) ◽  
pp. 500 ◽  
Author(s):  
Tandressa S. Berguetti ◽  
Lucas S. P. Quintaes ◽  
Thais Hancio Pereira ◽  
Marcela Robaina ◽  
André Cruz ◽  
...  
Keyword(s):  
Extracellular Vesicles ◽  
Cellular Proliferation ◽  
Proliferation Index ◽  
Necrosis Factor Alpha ◽  
P Glycoprotein ◽  
Tnf Α ◽  
Factor Alpha ◽  
Membrane Microparticles

P-glycoprotein (Pgp/ABCB1) overexpression is associated with multidrug resistance (MDR) phenotype and, consequently, failure in cancer chemotherapy. However, molecules involved in cell death deregulation may also support MDR. Tumor necrosis factor-alpha (TNF-α) is an important cytokine that may trigger either death or tumor growth. Here, we examined the role of cancer cells in self-maintenance and promotion of cellular malignancy through the transport of Pgp and TNF-α molecules by extracellular vesicles (membrane microparticles (MP)). By using a classical MDR model in vitro, we identified a positive correlation between endogenous TNF-α and Pgp, which possibly favored a non-cytotoxic effect of recombinant TNF-α (rTNF-α). We also found a positive feedback involving rTNF-α incubation and TNF-α regulation. On the other hand, rTNF-α induced a reduction in Pgp expression levels and contributed to a reduced Pgp efflux function. Our results also showed that parental and MDR cells spontaneously released MP containing endogenous TNF-α and Pgp. However, these MP were unable to transfer their content to non-cancer recipient cells. Nevertheless, MP released from parental and MDR cells elevated the proliferation index of non-tumor cells. Collectively, our results suggest that Pgp and endogenous TNF-α positively regulate cancer cell malignancy and contribute to changes in normal cell behavior through MP.

scholarly journals Effect of Mycobacterium bovis BCG Vaccinationon Mycobacterium-Specific Cellular Proliferation and TumorNecrosis Factor Alpha Production from Distinct Guinea PigLeukocytePopulations

2003 ◽  
Vol 71 (12) ◽  
pp. 7035-7042 ◽  
Author(s):  
Todd M. Lasco ◽  
Toshiko Yamamoto ◽  
Teizo Yoshimura ◽  
Shannon Sedberry Allen ◽  
Lynne Cassone ◽  
...  
Keyword(s):  
Guinea Pig ◽  
Mycobacterium Bovis ◽  
Cellular Proliferation ◽  
Strong Positive Correlation ◽  
Necrosis Factor Alpha ◽  
Alpha Production ◽  
Tnf Α ◽  
Factor Alpha ◽  
Mycobacterial Strain ◽  
Necrosis Factor

ABSTRACT In this study, we focused on three leukocyte-rich guinea pig cell populations, bronchoalveolar lavage (BAL) cells, resident peritoneal cells (PC), and splenocytes (SPC). BAL cells, SPC, and PC were stimulated either with live attenuated Mycobacterium tuberculosis H37Ra or with live or heat-killed virulent M. tuberculosis H37Rv (multiplicity of infection of 1:100). Each cell population was determined to proliferate in response to heat-killed virulent H37Rv, whereas no measurable proliferative response could be detected upon stimulation with live mycobacteria. Additionally, this proliferative capacity (in SPC and PC populations) was significantly enhanced upon prior vaccination with Mycobacterium bovis BCG. Accordingly, in a parallel set of experiments we found a strong positive correlation between production of antigen-specific bioactive tumor necrosis factor alpha (TNF-α) and prior vaccination with BCG. A nonspecific stimulus, lipopolysaccharide, failed to induce this effect on BAL cells, SPC, and PC. These results showed that production of bioactive TNF-α from mycobacterium-stimulated guinea pig cell cultures positively correlates with the vaccination status of the host and with the virulence of the mycobacterial strain.

Simulation stress model of the undersea environment activates the central nervous, neuroendocrine and immune systems and anxiety in rats

2020 ◽  
pp. 445-453
Author(s):  
Ying Tang ◽  
Ying-Xin Zou ◽  
Wei Fan ◽  
Shuang-Hong Chen ◽  
Yi-Qun Fang ◽  
...  
Keyword(s):  
Stress Responses ◽  
Interleukin 1 ◽  
Control Group ◽  
Stress Model ◽  
Necrosis Factor Alpha ◽  
Immune Systems ◽  
Tnf Α ◽  
The Central Nervous System ◽  
Factor Alpha ◽  
Necrosis Factor

The present study was designed to assess the stress responses to a simulation model of the undersea environment that is similar to some undersea working conditions such as submarine rescue, underwater salvage and underwater construction. Restraint, hyperbaric air and immersion were chosen to produce the simulation stress model in rats for four hours. Rats were randomized into five groups: control group, restraint (R) group, hyperbaric air (H) group, restraint plus hyperbaric air (RH) group, and restraint plus hyperbaric air plus immersion (RHI) group. The results showed that the responses to the simulation stress model of the undersea environment induced by R, H, RH and RHI involved the upregulated norepinephrine (NE), dopamine (DA) and 5-hydroxytryptamine (5-HT) of the central nervous system (CNS), upregulated adrenocorticotropic hormone (ACTH), corticosterone (CORT) and blood glucose of the neuroendocrine system, upregulated interleukin-1 (IL-1), interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-α) of the immune system, and increased anxiety in rats. Compared with hyperbaric air, restraint tended to activate stronger stress responses. Conclusively, this work established a simulation stress model of the undersea environment induced by restraint, hyperbaric air and immersion. It further provided experimental data of such a model that showed significant activation of the CNS, neuroendocrine and immune systems and anxiety in rats. In this experiment we provided an experimental basis for undersea work such as working aboard a submarine.

scholarly journals Reactive Astrocytes: Critical Players in the Development of Chronic Pain

2021 ◽  
Vol 12 ◽  
Author(s):  
James Tang ◽  
Mercedes Bair ◽  
Giannina Descalzi
Keyword(s):  
Central Nervous System ◽  
Chronic Pain ◽  
Nervous System ◽  
Synaptic Function ◽  
Necrosis Factor Alpha ◽  
Form And Function ◽  
Metabolic Coupling ◽  
The Central Nervous System ◽  
Factor Alpha ◽  
And Function

Chronic pain is associated with long term plasticity of nociceptive pathways in the central nervous system. Astrocytes can profoundly affect synaptic function and increasing evidence has highlighted how altered astrocyte activity may contribute to the pathogenesis of chronic pain. In response to injury, astrocytes undergo a shift in form and function known as reactive astrogliosis, which affects their release of cytokines and gliotransmitters. These neuromodulatory substances have been implicated in driving the persistent changes in central nociceptive activity. Astrocytes also release lactate which neurons can use to produce energy during synaptic plasticity. Furthermore, recent research has provided insight into lactate's emerging role as a signaling molecule in the central nervous system, which may be involved in directly modulating neuronal and astrocytic activity. In this review, we present evidence for the involvement of astrocyte-derived tumor necrosis factor alpha in pain-associated plasticity, in addition to research suggesting the potential involvement of gliotransmitters D-serine and adenosine-5′-triphosphate. We also discuss work implicating astrocyte-neuron metabolic coupling, and the possible role of lactate, which has been sparsely studied in the context of chronic pain, in supporting pathological changes in central nociceptive activity.

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