Influence of tumour necrosis factor-α, tumour necrosis factor-β and interferon-γ, separately and added together with interleukin-1 β, on the function of cultured human thyroid cells

1994 ◽  
Vol 143 (2) ◽  
pp. 359-365 ◽  
Author(s):  
Å K Rasmussen ◽  
L Kayser ◽  
U Feldt-Rasmussen ◽  
K Bendtzen
Keyword(s):  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Human Thyroid ◽  
Inhibitory Influence ◽  
Camp Production ◽  
Thyroid Cells ◽  
Tnf Α ◽  
Ifn Γ ◽  
High Concentrations ◽  
Necrosis Factor

Abstract Interleukin (IL)-1, tumour necrosis factor (TNF)-α and interferon (IFN)-γ have been demonstrated in thyroid tissue. We have previously shown that high concentrations of IL-1 inhibit and low concentrations stimulate human thyroid cell function in vitro. In the present study, TNF-α, TNF-β and IFN-γ all inhibited thyroglobulin (Tg) and cAMP production from cultured human thyroid cells. When TNF-α was added simultaneously with IL-1 β, the highest concentration of TNF-α (106 U/l) enhanced the inhibition of Tg and cAMP induced by IL-1β (1–105 U/1). TNF-β had no influence on IL-1β-induced inhibition. IFN-γ (104 U/1) added together with IL-1β in lower concentrations (1—102 U/l) stimulated cAMP production, while at high concentrations of IL-1β (105 U/1), IFN-γ enhanced the inhibitory influence of IL-1 β on Tg production. The hormones of the immune system, IL-1, TNF and IFN-γ, may thus contribute to the decreased thyroid function characteristic of some thyroid inflammatory diseases. Journal of Endocrinology (1994) 143, 359–365

scholarly journals Circulating tumour necrosis factor-α and interferon-γ are detectable during acute and convalescent parvovirus B19 infection and are associated with prolonged and chronic fatigue

2001 ◽  
Vol 82 (12) ◽  
pp. 3011-3019 ◽  
Author(s):  
Jonathan R. Kerr ◽  
Faraj Barah ◽  
Derek L. Mattey ◽  
Ian Laing ◽  
Stephen J. Hopkins ◽  
...  
Keyword(s):  
Virus Infection ◽  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Parvovirus B19 ◽  
Acute Infection ◽  
Tnf Α ◽  
Parvovirus B19 Infection ◽  
Ifn Γ ◽  
Necrosis Factor

To investigate whether cytokine responses may have a bearing on the symptoms and outcome of parvovirus B19 infection, circulating cytokines were measured during acute infection (n=51), follow-up of acute infection (n=39) and in normal healthy controls (n=50). At acute B19 virus infection (serum anti-B19 IgM-positive), patients ranged in age from 4 to 54 years, with a mean age of 28·2 years. The male:female ratio was 1:4·1 and symptoms were rash (n=15), arthralgia (n=31), fatigue (n=8), lymphadenopathy (n=4), foetal hydrops (n=3), transient aplastic crisis (n=2), neutropenia (n=2), myelodysplasia (n=1), thrombocytopenia (n=1) and pancytopenia (n=1). Of these patients, 39 were contacted after a follow-up period of 2–37 months (mean of 22·5 months). In comparison with normal controls, detectable IL-6 was associated with acute B19 virus infection (26%; P=0·0003), but not with follow-up (6%; P=0·16). Detection of interferon (IFN)-γ was associated with acute B19 virus infection (67%; P<0·0001) and follow-up (67%; P<0·0001). Detection of tumour necrosis factor (TNF)-α was associated with acute B19 virus infection (49%; P<0·0001) and follow-up (56%; P<0·0001). IL-1β was detected in acute infection (20%), but not at follow-up. At acute B19 virus infection, detection of serum/plasma IL-6 was associated with rheumatoid factor (P=0·038) and IFN-γ (⩾7 pg/ml) was associated with fatigue in those patients of ⩾15 years of age (P=0·022). At follow-up, fatigue was associated with IFN-γ (⩾7 pg/ml) and/or TNF-α (⩾40 pg/ml) (P=0·0275). Prolonged upregulation of serum IFN-γ and TNF-α appears to represent a consistent host response to symptomatic B19 virus infection.

scholarly journals Modulation of ACE-2 mRNA by inflammatory cytokines in human thyroid cells: a pilot study

Endocrine ◽  
2021 ◽  
Author(s):  
Francesca Coperchini ◽  
Gianluca Ricci ◽  
Laura Croce ◽  
Marco Denegri ◽  
Rubina Ruggiero ◽  
...  
Keyword(s):  
Inflammatory Cytokines ◽  
Combination Treatment ◽  
Primary Cultures ◽  
Human Thyroid ◽  
Thyroid Cell ◽  
Mrna Levels ◽  
Thyroid Cells ◽  
Tnf Α ◽  
Ifn Γ ◽  
Pro Inflammatory Cytokines

Abstract Introduction Angiotensin-converting-enzyme-2 (ACE-2) was demonstrated to be the receptor for cellular entry of SARS-CoV-2. ACE-2 mRNA was identified in several human tissues and recently also in thyroid cells in vitro. Purpose Aim of the present study was to investigate the effect of pro-inflammatory cytokines on the ACE-2 mRNA levels in human thyroid cells in primary cultures. Methods Primary thyroid cell cultures were treated with IFN-γ and TNF-α alone or in combination for 24 h. ACE-2 mRNA levels were measured by RT-PCR. As a control, the levels of IFN-γ inducible chemokine (CXCL10) were measured in the respective cell culture supernatants. Results The mean levels of ACE-2 mRNA increased after treatment with IFN-γ and TNF-α in all the thyroid cell preparations, while the combination treatment did not consistently synergically increase ACE-2-mRNA. At difference, CXCL10 was consistently increased by IFN-γ and synergically further increased by the combination treatment with IFN-γ + TNF-α, with respect to IFN-γ alone. Conclusions The results of the present study show that IFN-γ and, to a lesser extent TNF-α consistently increase ACE-2 mRNA levels in NHT primary cultures. More interestingly, the combined stimulation (proven to be effective according to the synergic effect registered for CXCL10) produces different responses in terms of ACE-2 mRNA modulation. These results would suggest that elevated levels of pro-inflammatory cytokines could facilitate the entering of the virus in cells by further increasing ACE-2 expression and/or account for the different degree of severity of SARS-COV-2 infection. This hypothesis deserves to be confirmed by further specific studies.

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 Pregnancy in Takayasu Arteritis Patients Exposed to Anti-Tumour Necrosis Factor (Anti-TNF)-α Therapy

2016 ◽  
Vol 2 (5) ◽  
pp. 96-98
Author(s):  
Valentina Canti ◽  
◽  
Elena Baldissera ◽  
Susanna Rosa ◽  
Giuseppe A. Ramirez ◽  
...  
Keyword(s):  
Tumour Necrosis Factor ◽  
Takayasu Arteritis ◽  
Tumour Necrosis ◽  
Tnf Α ◽  
Necrosis Factor
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