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.

scholarly journals P415 Paradoxical onset of Takayasu’s arteritis in patients with inflammatory bowel disease treated with anti-tumour necrosis factor-α agents

2021 ◽  
Vol 15 (Supplement_1) ◽  
pp. S422-S422
Author(s):  
Y Matsune ◽  
J Kouyama ◽  
Y Tsuru ◽  
K Shimizu ◽  
S Asami ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Clinical Features ◽  
Bowel Disease ◽  
Tumour Necrosis ◽  
Rare Complication ◽  
Tumour Necrosis Factor Α ◽  
Tnf Α ◽  
Inflammatory Bowel ◽  
Factor Α ◽  
Necrosis Factor

Abstract Background Takayasu’s arteritis (TA) is a rare complication associated with inflammatory bowel disease (IBD). TA is a granulomatous systemic vasculitis of uncertain aetiology affecting large arteries, predominantly the aorta and its main branches, leading to stenotic and expansible lesions. The estimated prevalence of coexisting of TA in patients with ulcerative colitis (UC) is 0.3%, and that in patients with Crohn’s disease (CD) is 0.1%. Anti-tumour necrosis factor-α (TNF-α) agents are used to treat both TA and IBD, although some patients with IBD paradoxically develop TA during treatment with anti-TNF-α agents. However, data regarding the incidence and clinical features of TA in such cases are lacking. This study was performed to clarify the prevalence, risk factors, and clinical features of TA that develops paradoxically during treatment with anti-TNF-α agents in patients with IBD. Methods Consecutive patients with IBD who were regularly seen at our centre, a tertiary IBD centre in Japan, from 2000 to 2019 were included in this retrospective single-centre study. We evaluated the prevalence of TA according to the presence or absence of treatment with anti-TNF-α agents and the patients’ clinical manifestations. Results Of 1846 patients with UC and 1249 patients with CD, 7 (0.23%) patients with UC developed TA. The prevalence of TA in patients treated with anti-TNF-α agents was significantly higher (4/254, 1.6%) than that in patients without anti-TNF-α agent treatment (3/1592, 0.19%) (p=0.0087, Fisher’s exact test). Among four patients with UC who paradoxically developed TA during treatment with anti-TNF-α agents, three (75%) received infliximab, one (25%) received adalimumab, and one (25%) received golimumab. One was male and three (75%) were female. The median interval from starting treatment with anti-TNF-α agents to diagnosis of TA was 49.0 (34–63) months. All patients had pancolitis as well as persistent active colitis resistant to anti-TNF-α antibody treatment. The treatments for TA administered after anti-TNF-α therapy were as follows: Two (50%) patients discontinued anti-TNF-α agent therapy, three (75%) were treated with prednisolone, and one (25%) received tocilizumab. No patient required an operation for TA. Conclusion To our knowledge, this is the first study to show the prevalence and clinical features of TA in patients with IBD following administration of anti-TNF-α agent therapy. Although TA is a rare complication, our results suggest that it can develop as paradoxical reaction following administration of anti-TNF-α agents.

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

Anti-tumour necrosis factor-α antibodies and B cell homeostasis in human inflammatory bowel diseases

2018 ◽  
Vol 54 ◽  
pp. 329-335 ◽  
Author(s):  
Caterina Defendenti ◽  
Fabiola Atzeni ◽  
Sergio Malandrin ◽  
Sandro Ardizzone ◽  
Piero Luigi Almasio ◽  
...  
Keyword(s):  
B Cell ◽  
Tumour Necrosis Factor ◽  
Inflammatory Bowel Diseases ◽  
Tumour Necrosis ◽  
Tumour Necrosis Factor Α ◽  
Bowel Diseases ◽  
Inflammatory Bowel ◽  
B Cell Homeostasis ◽  
Factor Α ◽  
Necrosis Factor

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).

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