scholarly journals Dimethylfumarate inhibits microglial and astrocytic inflammation by suppressing the synthesis of nitric oxide, IL-1β, TNF-α and IL-6 in an in-vitro model of brain inflammation

2010 ◽  
Vol 7 (1) ◽  
pp. 30 ◽  
Author(s):  
Henrik Wilms ◽  
Jobst Sievers ◽  
Uta Rickert ◽  
Martin Rostami-Yazdi ◽  
Ulrich Mrowietz ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
In Vitro Model ◽  
Brain Inflammation ◽  
Tnf Α ◽  
Vitro Model

scholarly journals In Vitro Model of Mycobacterial Growth Arrest Using Nitric Oxide with Limited Air

2008 ◽  
Vol 53 (1) ◽  
pp. 157-161 ◽  
Author(s):  
Syed Hussain ◽  
Muhammad Malik ◽  
Lanbo Shi ◽  
Maria Laura Gennaro ◽  
Karl Drlica
Keyword(s):  
Nitric Oxide ◽  
In Vitro Model ◽  
Transition Period ◽  
Time Lag ◽  
Growth Arrest ◽  
Ring Structure ◽  
Time Lags ◽  
Vitro Model ◽  
Mycobacterial Growth

ABSTRACT An in vitro model of mycobacterial growth arrest was developed using Mycobacterium bovis BCG. When an exponentially growing culture was transferred to an evacuated tube, growth continued; treatment with a source of nitric oxide (diethylenetriamine-nitric oxide adduct [DETA-NO] at 50 μM) halted growth immediately, and aeration restored growth. When the period of growth arrest exceeded 4 h, a time lag occurred before aeration could restore growth. The lag time was maximal (24 h) after 16 h of growth arrest. These time lags indicated that one transition period was required for cells to achieve full arrest of growth and another for them to recover fully from growth arrest. DETA-NO-induced growth arrest failed to protect from the lethal effects of anaerobic shock, which caused rapid lysis of both growing and growth-arrested cells. While growth arrest had little effect on the lethal action of rifampin, it eliminated isoniazid lethality. Growth arrest reduced but did not eliminate fluoroquinolone lethality. Two fluoroquinolones, moxifloxacin and gatifloxacin, were equally lethal to exponentially growing cells, but moxifloxacin was more active during growth arrest. This difference is attributed to the fluoroquinolone C-7 ring structure, the only difference between the compounds. Collectively these data characterize a new system for halting mycobacterial growth that may be useful for evaluating new antituberculosis agents.

TNF-α Induces MMP2 Gelatinase Activity and MT1-MMP Expression in an In Vitro Model of Nucleus Pulposus Tissue Degeneration

Spine ◽  
2008 ◽  
Vol 33 (4) ◽  
pp. 356-365 ◽  
Author(s):  
Cheryle A. Séguin ◽  
Robert M. Pilliar ◽  
Joseph A. Madri ◽  
Rita A. Kandel
Keyword(s):  
Nucleus Pulposus ◽  
In Vitro Model ◽  
Gelatinase Activity ◽  
Nucleus Pulposus Tissue ◽  
Tissue Degeneration ◽  
Tnf Α ◽  
Vitro Model

Induction of osteoclastogenesis in an in vitro model of Gaucher disease is mediated by T cells via TNF-α

Gene ◽  
2012 ◽  
Vol 509 (1) ◽  
pp. 51-59 ◽  
Author(s):  
Juan M. Mucci ◽  
Romina Scian ◽  
Pablo N. De Francesco ◽  
Florencia Suqueli García ◽  
Romina Ceci ◽  
...  
Keyword(s):  
T Cells ◽  
Gaucher Disease ◽  
In Vitro Model ◽  
Tnf Α ◽  
Vitro Model

scholarly journals Aβ oligomers trigger necroptosis-mediated neurodegeneration via microglia activation in Alzheimer′s disease.

2021 ◽  
Author(s):  
Natalia Salvadores ◽  
Ines Moreno ◽  
Nazareth Gamez ◽  
Gabriel Quiroz ◽  
Laura Vegas ◽  
...  
Keyword(s):  
Microglial Activation ◽  
In Vitro Model ◽  
Amyloid Β ◽  
Etiologic Agent ◽  
Neuron Death ◽  
Aβ Oligomers ◽  
Therapeutic Implications ◽  
Tnf Α ◽  
Vitro Model

Alzheimer′s disease (AD) is a major adult-onset neurodegenerative condition with no available treatment. Compelling reports point amyloid-β (Aβ) as the main etiologic agent that triggers AD. Although there is extensive evidence of a detrimental crosstalk between Aβ and microglia that contributes to neuroinflammation in AD, the exact mechanism leading to neuron death remains unknown. Using postmortem human AD brain tissue, we show that Aβ oligomers (Aβo) colocalize with the necroptosis effector pMLKL. Moreover, we found that the burden of Aβo correlates with the expression of key markers of necroptosis activation. Additionally, inhibition of necroptosis by pharmacological or genetic means, reduce neurodegeneration and memory impairment triggered by Aβo in mice. Since microglial activation is emerging as a central driver for AD pathogenesis, we then tested the contribution of microglia to the mechanism of Aβo-mediated necroptosis activation in neurons. Using an in vitro model, we show that conditioned medium from Aβo-stimulated microglia elicited necroptosis in neurons through activation of TNF-α signaling, triggering extensive neurodegeneration. Notably, necroptosis inhibition provided significant neuronal protection. Together, these findings suggest that Aβo-mediated microglia stimulation in AD contributes to necroptosis activation in neurons and neurodegeneration. As necroptosis is a druggable degenerative mechanism, our findings might have important therapeutic implications to prevent the progression of AD.

GSK-3 mediates differentiation and activation of proinflammatory dendritic cells

Blood ◽  
2006 ◽  
Vol 109 (4) ◽  
pp. 1584-1592 ◽  
Author(s):  
Elena Rodionova ◽  
Michael Conzelmann ◽  
Eugene Maraskovsky ◽  
Michael Hess ◽  
Michael Kirsch ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
In Vitro Model ◽  
Glycogen Synthase ◽  
Human Monocyte ◽  
Glycogen Synthase Kinase 3 ◽  
Inhibitory Effects ◽  
Tnf Α ◽  
Vitro Model

Abstract The key components of the intracellular molecular network required for the expression of a specific function of dendritic cells (DCs) are as yet undefined. Using an in vitro model of human monocyte-derived DC differentiation, this study investigates the role of glycogen synthase kinase 3 (GSK-3), a multifunctional enzyme critical for cellular differentiation, apoptosis, self-renewal, and motility, in this context. We demonstrate that GSK-3 (1) inhibits macrophage development during differentiation of DCs, (2) is constitutively active in immature DCs and suppresses spontaneous maturation, and (3) acquires a proinflammatory functional status mediating high levels of IL-12, IL-6, and TNF-α secretion, and partially inhibits IL-10 in the context of DC activation. In particular, GSK-3 enhances IL-12p35 mRNA expression and thus the production of the proinflammatory cytokine IL-12p70 by integrating the activities of other kinases priming GSK-3 targets and the inhibitory effects of Akt-1. GSK-3 may therefore act as a key integrator of activating and inhibitory pathways involved in proinflammatory DC differentiation and activation.

Interleukin-8 stimulates the migration of human colonic epithelial cells in vitro

1999 ◽  
Vol 97 (3) ◽  
pp. 385-390 ◽  
Author(s):  
Andrew J. WILSON ◽  
Keith BYRON ◽  
Peter R. GIBSON
Keyword(s):  
Cell Migration ◽  
Epithelial Cells ◽  
In Vitro Model ◽  
Interleukin 8 ◽  
Colonic Epithelium ◽  
Dependent Manner ◽  
Colonic Epithelial Cells ◽  
Tnf Α ◽  
Vitro Model

The migration of colonic epithelial cells (restitution) is an important event in the repair of mucosal injuries. Interleukin-8 (IL-8) is a physiological initiator of the chemotactic migration of leucocytes. This study aimed to determine whether IL-8 had a similar effect on migration in an in vitro model of wounded colonic epithelium. Cell migration over 24 h was assessed in circular wounds made in confluent monolayers of the human colon cancer cell line LIM1215. This migration was stimulated in a concentration-dependent manner by IL-8, with maximal effects of approx. 1.75-fold above basal migration. The motogenic effect of IL-8 was mediated independently of effects on cell proliferation. In contrast, it was partially dependent upon gene transcription and protein synthesis and involved the activation of pertussis-toxin-sensitive G-proteins. The short-chain fatty acids, acetate, propionate, butyrate and valerate, the activator of protein kinase C (phorbol-12-myristate-13-acetate) and tumour necrosis factor-α (TNF-α) all stimulated the secretion of IL-8. However, only the motogenic effect of TNF-α was dependent upon IL-8. In conclusion, IL-8 stimulated cell migration in an in vitro model of colonic epithelium, whereas the motogenic effect of at least one physiologically relevant factor was dependent upon an increase in its endogenous levels. If IL-8 stimulates colonic epithelial restitution in vivo, this would have ramifications for the control of repair processes following wounding of the colonic mucosa.

Induction of Arginase II mRNA by Nitric Oxide Using an In Vitro Model of Gyrate Atrophy of Choroid and Retina

2011 ◽  
Vol 52 (3) ◽  
pp. 1493 ◽  
Author(s):  
Masayuki Ohnaka ◽  
Emiko Okuda-Ashitaka ◽  
Shiho Kaneko ◽  
Akira Ando ◽  
Masahide Maeda ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
In Vitro Model ◽  
Gyrate Atrophy ◽  
Arginase Ii ◽  
Vitro Model
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