scholarly journals Surface engineering of porous silicon to optimise therapeutic antibody loading and release

2015 ◽  
Vol 3 (20) ◽  
pp. 4123-4133 ◽  
Author(s):  
Steven J. P. McInnes ◽  
Chris T. Turner ◽  
Sameer A. Al-Bataineh ◽  
Marta J. I. Airaghi Leccardi ◽  
Yazad Irani ◽  
...  
Keyword(s):  
Porous Silicon ◽  
Proinflammatory Cytokine ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Surface Engineering ◽  
Chronic Wounds ◽  
Tnf Α ◽  
Cytokine Tumor Necrosis Factor ◽  
Factor Α ◽  
Necrosis Factor

Infliximab antibodies released from porous silicon microparticles can sequester the proinflammatory cytokine, tumor necrosis factor-α (TNF-α), which is elevated in uveitis and non-healing chronic wounds.

scholarly journals iRhom2 and TNF: Partners or enemies?

2019 ◽  
Vol 12 (605) ◽  
pp. eaaz0444 ◽  
Author(s):  
Marina Badenes ◽  
Colin Adrain
Keyword(s):  
Hepatic Stellate Cells ◽  
Proinflammatory Cytokine ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Stellate Cells ◽  
Protective Role ◽  
Tnf Α ◽  
Cytokine Tumor Necrosis Factor ◽  
Factor Α ◽  
Necrosis Factor

iRhom2 is an essential cofactor for ADAM17, the metalloprotease that sheds both the proinflammatory cytokine tumor necrosis factor–α (TNF-α) and TNF receptors (TNFRs) from the cell surface. In this issue of Science Signaling, Sundaram et al. demonstrate a protective role for iRhom2 in promoting ADAM17-mediated shedding of TNFRs in hepatic stellate cells, which reduces TNFR signaling and liver fibrosis in response to injury.

scholarly journals The proinflammatory cytokine tumor necrosis factor-α excites subfornical organ neurons

2017 ◽  
Vol 118 (3) ◽  
pp. 1532-1541 ◽  
Author(s):  
Nick J. Simpson ◽  
Alastair V. Ferguson
Keyword(s):  
Tumor Necrosis Factor ◽  
Proinflammatory Cytokine ◽  
Potassium Current ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Subfornical Organ ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

Tumor necrosis factor-α (TNF-α) is a proinflammatory cytokine implicated in cardiovascular and autonomic regulation via actions in the central nervous system. TNF-α−/− mice do not develop angiotensin II (ANG II)-induced hypertension, and administration of TNF-α into the bloodstream of rats increases blood pressure and sympathetic tone. Recent studies have shown that lesion of the subfornical organ (SFO) attenuates the hypertensive and autonomic effects of TNF-α, while direct administration of TNF-α into the SFO increases blood pressure, suggesting the SFO to be a key site for the actions of TNF-α. Therefore, we used patch-clamp techniques to examine both acute and long-term effects of TNF-α on the excitability of Sprague-Dawley rat SFO neurons. It was observed that acute bath application of TNF-α depolarized SFO neurons and subsequently increased action potential firing rate. Furthermore, the magnitude of depolarization and the proportion of depolarized SFO neurons were concentration dependent. Interestingly, following 24-h incubation with TNF-α, the basal firing rate of the SFO neurons was increased and the rheobase was decreased, suggesting that TNF-α elevates SFO neuron excitability. This effect was likely mediated by the transient sodium current, as TNF-α increased the magnitude of the current and lowered its threshold of activation. In contrast, TNF-α did not appear to modulate either the delayed rectifier potassium current or the transient potassium current. These data suggest that acute and long-term TNF-α exposure elevates SFO neuron activity, providing a basis for TNF-α hypertensive and sympathetic effects. NEW & NOTEWORTHY Considerable recent evidence has suggested important links between inflammation and the pathological mechanisms underlying hypertension. The present study describes cellular mechanisms through which acute and long-term exposure of tumor necrosis factor-α (TNF-α) influences the activity of subfornical organ neurons by modulating the voltage-gated transient Na+ current. This provides critical new information regarding the specific pathological mechanisms through which inflammation and TNF-α in particular may result in the development of hypertension.

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