scholarly journals Association of tumour necrosis factor-α (TNF-α) gene polymorphisms (-308 G>A and -238 G>A) and the risk of severe dengue: A meta-analysis and trial sequential analysis

PLoS ONE ◽  
2018 ◽  
Vol 13 (10) ◽  
pp. e0205413
Author(s):  
Cho Naing ◽  
Norah Htet Htet ◽  
Wong Siew Tung ◽  
Arun Kumar Basavaraj ◽  
Joon Wah Mak
Keyword(s):  
Gene Polymorphisms ◽  
Tumour Necrosis ◽  
Sequential Analysis ◽  
Meta Analysis ◽  
Severe Dengue ◽  
Trial Sequential Analysis ◽  
Tumour Necrosis Factor Α ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

scholarly journals Can coenzyme Q10 supplementation effectively reduce human tumour necrosis factor-α and interleukin-6 levels in chronic diseases? Protocol for a systematic review and meta-analysis of randomised controlled trials

BMJ Open ◽  
2017 ◽  
Vol 7 (10) ◽  
pp. e016841 ◽  
Author(s):  
Farnaz Farsi ◽  
Javad Heshmati ◽  
Leila Janani ◽  
Pardis Irandoost ◽  
Naeimeh Mesri Alamdari ◽  
...  
Keyword(s):  
Systematic Review ◽  
Coenzyme Q10 ◽  
Interleukin 6 ◽  
Tumour Necrosis ◽  
Meta Analysis ◽  
Tumour Necrosis Factor Α ◽  
Tnf Α ◽  
Randomised Controlled ◽  
Factor Α ◽  
Necrosis Factor

IntroductionInflammation, as a critical factor, can cause numerous chronic diseases by creating various proinflammatory cytokines. Coenzyme Q10 (CoQ10) can potentially exert an anti-inflammatory agent; in turn, this agent can reduce the systemic inflammatory response. The aims of this study are to conduct a comprehensive systematic review and a meta-analysis for the determination of the CoQ10 efficacy on the changes in serum interleukin-6 (IL-6) and the tumour necrosis factor-α (TNF-α) levels in unhealthy subjects.Method and analysisWe will conduct an electronic search for articles published between January 1990 and January 2017 using a prespecified search strategy in MEDLINE, SCOPUS, EMBASE, CENTRAL and Web of Science.Our search will focus only on randomised controlled clinical trials in unhealthy subjects that employ either a parallel or a crossover design; this search will involve concurrent control groups. The primary outcomes of the literature are to determine the CoQ10 efficacy on the changes in the serum IL-6 and the TNF-α levels in unhealthy subjects. Secondary outcomes such as body mass index, serum adiponectin and high-sensitivity C-reactive protein levels, lipid profile and the heterogeneity assessment of the primary studies will be evaluated. The stages of screen articles, the extracts of relevant data and the assessment of study quality using the Cochrane risk of bias tool will be conducted independently by the two reviewers. Any disagreement will be resolved by discussion with a third person. If the number of eligible studies is sufficient, we will carry out a meta-analysis according to both outcomes.Ethics and disseminationThis study is the protocol for a systematic review and no ethics approval is needed. The findings from the full systematic review will be published in a peer-reviewed journal, and they will also be exhibited at national/international academic and clinical conferences.Trial registration numberCRD42016052200.

Differential effect of selective block of α2-adrenoreceptors on plasma levels of tumour necrosis factor-α, interleukin-6 and corticosterone induced by bacterial lipopolysaccharide in mice

1995 ◽  
Vol 144 (3) ◽  
pp. 457-462 ◽  
Author(s):  
G Haskó ◽  
I J Elenkov ◽  
V Kvetan ◽  
E S Vizi
Keyword(s):  
Tumour Necrosis Factor ◽  
Interleukin 6 ◽  
Plasma Levels ◽  
Tumour Necrosis ◽  
Endotoxin Shock ◽  
Bacterial Lipopolysaccharide ◽  
Tumour Necrosis Factor Α ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

Abstract The effect of selective block of α2-adrenoreceptors on plasma levels of tumour necrosis factor-α (TNF-α), interleukin-6 (IL-6) and corticosterone induced by bacterial lipopolysaccharide (LPS) was investigated in mice using ELISA and RIA. It was found that the LPS-induced TNF-α response was significantly blunted in mice pretreated with CH-38083, a novel and highly selective α2-adrenoreceptor antagonist (the α2/α1 ratio is >2000). In contrast, LPS-induced increases in both corticosterone and IL-6 plasma levels were further increased by CH-38083. Since it has recently been shown that the selective block of α2-adrenoreceptors located on noradrenergic axon terminals resulted in an increase in the release of noradrenaline (NA), both in the central and peripheral nervous systems, and, in our experiments, that propranolol prevented the effect of α2-adrenoreceptor blockade on TNF-α plasma levels induced by LPS, it seems likely that the excessive stimulation by NA of β-adrenoreceptors located on cytokine-secreting immune cells is responsible for this action. Since it is generally accepted that increased production of TNF-α is involved in the pathogenesis of inflammation and endotoxin shock on the one hand, and corticosterone and even IL-6 are known to possess anti-inflammatory properties on the other hand, it is suggested that the selective block of α2-adrenoreceptors might be beneficial in the treatment of inflammation and/or endotoxin shock. Journal of Endocrinology (1995) 144, 457–462

scholarly journals Intracellular NAD+ levels are associated with LPS-induced TNF-α release in pro-inflammatory macrophages

2016 ◽  
Vol 36 (1) ◽  
Author(s):  
Abbas Jawad Al-Shabany ◽  
Alan John Moody ◽  
Andrew David Foey ◽  
Richard Andrew Billington
Keyword(s):  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Inflammatory Cytokine ◽  
Bacterial Lipopolysaccharide ◽  
Tumour Necrosis Factor Α ◽  
Tnf Α ◽  
Factor Α ◽  
Inflammatory Macrophages ◽  
Inflammatory Macrophage ◽  
Necrosis Factor

Bacterial lipopolysaccharide induces changes in intracellular NAD+ levels in a pro-inflammatory, but not an anti-inflammatory, macrophage model that are correlated with the release of the pro-inflammatory cytokine tumour necrosis factor-α (TNF-α).

scholarly journals Tumour necrosis factor-α mediates blood—brain barrier damage in HIV-1 infection of the central nervous system

1992 ◽  
Vol 1 (3) ◽  
pp. 191-196 ◽  
Author(s):  
M. K. Sharief ◽  
M. Ciardi ◽  
E. J. Thompson ◽  
F. Sorice ◽  
F. Rossi ◽  
...  
Keyword(s):  
Blood Brain Barrier ◽  
Tumour Necrosis ◽  
Brain Barrier ◽  
Tumour Necrosis Factor Α ◽  
Blood Brain ◽  
Tnf Α ◽  
Factor Α ◽  
Hiv 1 ◽  
Blood Brain Barrier Damage ◽  
Necrosis Factor

The pathogenesis of brain inflammation and damage by human immunodeficiency virus (HIV) infection is unclear. Because blood–brain barrier damage and impaired cerebral perfusion are common features of HIV-1 infection, we evaluated the role of tumour necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) in mediating disruption of the blood–brain barrier. Levels of TNF-α were more elevated in cerebrospinal fluid (CSF) than in serum of HIV-1 infected patients and were mainly detected in those patients who had neurologic involvement. Intrathecal TNF-α levels correlated with signs of blood–brain barrier damage, manifested by high CSF to serum albumin quotient, and with the degree of barrier impairment. In contrast, intrathecal IL-1β levels did not correlate with blood-brain barrier damage in HIV-1 infected patients. TNF-α seems to be related to active neural inflammation and to blood–brain barrier damage. The proinflammatory effects of TNF-α in the nervous system are dissociated from those of IL-1β.

Effects of tumor necrosis factor α on leptin-sensitive intestinal vagal mechanoreceptors in the cat

2013 ◽  
Vol 91 (11) ◽  
pp. 941-950 ◽  
Author(s):  
Nathalie Quinson ◽  
Véronique Vitton ◽  
Michel Bouvier ◽  
Jean-Charles Grimaud ◽  
Anne Abysique
Keyword(s):  
Tumour Necrosis ◽  
Discharge Frequency ◽  
Tumour Necrosis Factor Α ◽  
Tnf Α ◽  
Inflammatory Bowel ◽  
Pre Treatment ◽  
Factor Α ◽  
Necrosis Factor

The involvement of tumour necrosis factor α (TNF-α) in inflammatory bowel disease (IBD) has been established, and anti-TNF-α has been suggested as a therapeutic approach for the treatment of these pathologies. We studied the effects of TNF-α on leptin-sensitive intestinal vagal units to determine whether TNF-α exerts its effects through the intestinal vagal mechanoreceptors and to investigate its interactions with substances regulating food intake. The activity of intestinal vagal mechanoreceptors was recorded via microelectrodes implanted into the nodose ganglion in anesthetized cats. TNF-α (1 μg, i.a.) increased the discharge frequency of leptin-activated units (type 1 units; P < 0.05) and had no effect on the discharge frequency of leptin-inhibited units (type 2 units). When TNF-α was administered 20 min after sulfated cholecystokinin-8 (CCK), its excitatory effects on type 1 units were significantly enhanced (P < 0.0001) and type 2 units were significantly (P < 0.05) activated. Pre-treatment with Il-1ra (250 μg, i.a.) blocked the excitatory effects of TNF-α on type 1 units whereas the excitatory effects of TNF-α administration after CCK treatment on type 2 units were not modified. The activation of leptin-sensitive units by TNF-α may explain, at least in part, the weight loss observed in IBD.

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