Bovine Adrenal Cells Secrete Interleukin-6 and Tumor Necrosis Factor in Vitro

2000 ◽  
Vol 118 (2) ◽  
pp. 249-261 ◽  
Author(s):  
Gerald B. Call ◽  
Omar F. Husein ◽  
Christopher J. McIlmoil ◽  
Andrew Adams ◽  
Richard A. Heckmann ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Interleukin 6 ◽  
Tumor Necrosis ◽  
Adrenal Cells ◽  
Necrosis Factor

Dopamine increases interleukin 6 release and inhibits tumor necrosis factor release from rat adrenal zona glomerulosa cells in vitro

1996 ◽  
Vol 134 (5) ◽  
pp. 610-616 ◽  
Author(s):  
Paul K Ritchie ◽  
Marilyn Ashby ◽  
Heather H Knight ◽  
Allan M Judd
Keyword(s):  
Tumor Necrosis Factor ◽  
Interleukin 6 ◽  
Tumor Necrosis ◽  
Zona Glomerulosa ◽  
Adrenal Cells ◽  
Glomerulosa Cells ◽  
Necrosis Factor ◽  
Factor Release ◽  
Zona Glomerulosa Cells

Ritchie PK, Ashby M, Knight HH, Judd AM. Dopamine increases interleukin 6 release and inhibits tumor necrosis factor release from rat adrenal zona glomerulosa cells in vitro. Eur J Endocrinol 1996:134:610–6. ISSN 0804–4643 Interleukin 6 (IL-6) and tumor necrosis factor (TNF) are released from the zona glomerulosa of rat adrenal glands. The release of these cytokines from adrenal cells is regulated by interleukin 1β (IL-1β) and lipopolysaccharide (LPS), which are involved in the immune and inflammatory responses. Adrenocorticotropic hormone (ACTH) and angiotensin II, hormones that regulate the adrenal cortex, likewise regulate release of cytokines from adrenal glands. Dopamine inhibits aldosterone release from the adrenal cortex. Therefore, effects of dopamine on IL-6 and TNF release from rat adrenal zona glomerulosa were investigated. Primary cultures of rat adrenal zona glomerulosa cells were exposed to test agents and IL-6 and TNF release determined by the 7TD1 and WEHI bioassays, respectively. Dopamine increased basal IL-6 release and potentiated IL-6 release stimulated by ACTH, LPS or IL-1β. Dopamine inhibited basal and secretagogue-stimulated (LPS and IL-1β) TNF release. These effects of dopamine were mediated by D2 receptors because N-04 37, a D2 agonist, had effects on TNF and IL-6 release identical to those of dopamine. Therefore, dopamine, through D2 receptors, regulates the release of IL-6 and TNF from adrenal cells. Because TNF and IL-6 regulate adrenal steroid release, these cytokines may serve as autocrine or paracrine mediators of adrenal gland function. Allan M Judd, Department of Zoology, Brigham Young University, Provo, UT 84602, USA

Interleukin-6 and tumor necrosis factor α levels after bisphosphonates treatment in vitro and in patients with malignancy

Bone ◽  
1996 ◽  
Vol 18 (2) ◽  
pp. 133-139 ◽  
Author(s):  
A. Sauty ◽  
M. Pecherstorfer ◽  
I. Zimmer-Roth ◽  
P. Fioroni ◽  
L. Juillerat ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Interleukin 6 ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Factor Α ◽  
Necrosis Factor

In Vitro Acute Effects of Tobacco Smoke on Tumor Necrosis Factor a and Interleukin-6 Production by Alveolar Macrophages

1993 ◽  
Vol 19 (3) ◽  
pp. 345-359 ◽  
Author(s):  
VÉRonique Dubar ◽  
Philippe Gosset ◽  
Colette Aerts ◽  
Cyr Voisin ◽  
Benoit Wallaert ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tobacco Smoke ◽  
Alveolar Macrophages ◽  
Interleukin 6 ◽  
Tumor Necrosis ◽  
Acute Effects ◽  
Necrosis Factor

scholarly journals Combination of Tumor Necrosis Factor α and Interleukin-6 Induces Mouse Osteoclast-like Cells With Bone Resorption Activity Both In Vitro and In Vivo

2013 ◽  
Vol 66 (1) ◽  
pp. 121-129 ◽  
Author(s):  
Kazuhiro Yokota ◽  
Kojiro Sato ◽  
Takashi Miyazaki ◽  
Hideki Kitaura ◽  
Hisako Kayama ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Bone Resorption ◽  
Interleukin 6 ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Factor Α ◽  
Necrosis Factor

Interleukin-10 inhibits polymethylmethacrylate particle induced interleukin-6 and tumor necrosis factor-α release by human monocyte/macrophages in vitro

Biomaterials ◽  
2001 ◽  
Vol 22 (15) ◽  
pp. 2067-2073 ◽  
Author(s):  
Michael C.D. Trindade ◽  
Martin Lind ◽  
Yasuharu Nakashima ◽  
Doohoon Sun ◽  
Stuart B. Goodman ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Interleukin 6 ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Human Monocyte ◽  
Interleukin 10 ◽  
Factor Α ◽  
Necrosis Factor

scholarly journals Krüppel-Like Factor 4 Is a Regulator of Proinflammatory Signaling in Fibroblast-Like Synoviocytes through Increased IL-6 Expression

2016 ◽  
Vol 2016 ◽  
pp. 1-13 ◽  
Author(s):  
Xinjing Luo ◽  
Jie Chen ◽  
Jianwei Ruan ◽  
Yongfeng Chen ◽  
Xuanrong Mo ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Interleukin 6 ◽  
Tumor Necrosis ◽  
Vital Role ◽  
Cytokine Tumor Necrosis Factor ◽  
Synovial Tissues ◽  
Necrosis Factor ◽  
Fibroblast Like Synoviocytes

Human fibroblast-like synoviocytes play a vital role in joint synovial inflammation in rheumatoid arthritis (RA). Proinflammatory cytokines induce fibroblast-like synoviocyte activation and dysfunction. The inflammatory mediator Krüppel-like factor 4 is upregulated during inflammation and plays an important role in endothelial and macrophage activation during inflammation. However, the role of Krüppel-like factor 4 in fibroblast-like synoviocyte activation and RA inflammation remains to be defined. In this study, we identify the notion that Krüppel-like factor 4 is higher expressed in synovial tissues and fibroblast-like synoviocytes from RA patients than those from osteoarthritis patients.In vitro, the expression of Krüppel-like factor 4 in RA fibroblast-like synoviocytes is induced by proinflammatory cytokine tumor necrosis factor-α. Overexpression of Krüppel-like factor 4 in RA fibroblast-like synoviocytes robustly induced interleukin-6 production in the presence or absence of tumor necrosis factor-α. Conversely, knockdown of Krüppel-like factor 4 markedly attenuated interleukin-6 production in the presence or absence of tumor necrosis factor-α. Krüppel-like factor 4 not only can bind to and activate the interleukin-6 promoter, but also may interact directly with nuclear factor-kappa B. These results suggest that Krüppel-like factor 4 may act as a transcription factor mediating the activation of fibroblast-like synoviocytes in RA by inducing interleukin-6 expression in response to tumor necrosis factor-α.

scholarly journals Tiazofurin modulates lipopolysaccharide-activated microglia in vitro

2014 ◽  
Vol 66 (4) ◽  
pp. 1633-1640 ◽  
Author(s):  
Danijela Savic ◽  
Irena Lavrnja ◽  
Sanja Dacic ◽  
Ivana Bjelobaba ◽  
Nadezda Nedeljkovic ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Interleukin 6 ◽  
Tumor Necrosis ◽  
Interleukin 1 ◽  
Interleukin 10 ◽  
Antitumor Action ◽  
Activated Microglia ◽  
Anti Inflammatory ◽  
Necrosis Factor

Tiazofurin is a purine nucleoside analogue, with a broad spectrum of antitumoral and anti-inflammatory properties. In the present study, we have investigated the effect of tiazofurin on microglial inflammatory response to lipopolysaccharide in vitro. The cytotoxic effect of the drug was examined by sulforhodamine B assay. The Griess method was used to quantify nitrite production. Microglial morphology was assessed by measuring cell body size. Release of the pro-inflammatory cytokines, tumor necrosis factor-?, interleukin-1?, interleukin-6, and the anti-inflammatory cytokine interleukin- 10, were evaluated by enzyme-linked immunosorbent assay. Our data showed that tiazofurin decreased the number of activated microglia, lowered nitric oxide production and reduced the average cell surface of these cells. Tiazofurin reduced tumor necrosis factor-?, interleukin-6 and increased interleukin-10 secretion. Conversely, this drug promoted the release of interleukin-1?. Results obtained in this study indicate that TR displayed both anti- and pro-inflammatory modulation of activated microglia that could be relevant for its antitumor action within the central nervous system.

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