Novel Aspects of Cytokine Action in Porcine Uterus – Endometrial and Myometrial Production of Estrone (E1) in the Presence of Interleukin 1β (IL1β), Interleukin 6 (IL6) and Tumor Necrosis Factor (TNF α) –in Vitro Study

2013 ◽  
Vol 61 (3) ◽  
pp. 253-261 ◽  
Author(s):  
Anita Franczak ◽  
Bartosz Wojciechowicz ◽  
Genowefa Kotwica
Keyword(s):  
Tumor Necrosis Factor ◽  
Interleukin 6 ◽  
Tumor Necrosis ◽  
In Vitro Study ◽  
Vitro Study ◽  
Interleukin 1Β ◽  
Tnf Α ◽  
Necrosis Factor

scholarly journals Tumor Necrosis Factor α and Interleukin-1β Acutely Inhibit AgRP Neurons in the Arcuate Nucleus of the Hypothalamus

2020 ◽  
Vol 21 (23) ◽  
pp. 8928
Author(s):  
Fernanda M. Chaves ◽  
Naira S. Mansano ◽  
Renata Frazão ◽  
Jose Donato
Keyword(s):  
Tumor Necrosis Factor ◽  
Interleukin 6 ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Interleukin 1Β ◽  
Low Grade ◽  
Membrane Excitability ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

Obesity-associated low-grade inflammation favors weight gain, whereas systemic infection frequently leads to anorexia. Thus, inflammatory signals can either induce positive or negative energy balance. In this study, we used whole-cell patch-clamp to investigate the acute effects of three important proinflammatory cytokines, tumor necrosis factor α (TNF-α), interleukin-6, and interleukin-1β (IL-1β) on the membrane excitability of agouti-related peptide (AgRP)- or proopiomelanocortin (POMC)-producing neurons. We found that both TNF-α and IL-1β acutely inhibited the activity of 35–42% of AgRP-producing neurons, whereas very few POMC neurons were depolarized by TNF-α. Interleukin-6 induced no acute changes in the activity of AgRP or POMC neurons. Our findings indicate that the effect of TNF-α and IL-1β, especially on the activity of AgRP-producing neurons, may contribute to inflammation-induced anorexia observed during acute inflammatory conditions.

Serum Levels of Tumor Necrosis Factor-α (TNF-α), Interleukin-6 (IL-6), and Interleukin-1β (IL-1β) in Dengue-Infected Patients

1993 ◽  
Vol 48 (3) ◽  
pp. 324-331 ◽  
Author(s):  
Didier Hober ◽  
Bertrand Roblin ◽  
Robert Vergez-Pascal ◽  
Gerard Granic ◽  
Michele Maniez-Montreuil ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Interleukin 6 ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Serum Levels ◽  
Interleukin 1Β ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

scholarly journals Aktivitas imunomodulator ekstrak rumput laut

2020 ◽  
Vol 7 (2) ◽  
pp. 79
Author(s):  
Erniati Erniati ◽  
Riri Ezraneti
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Interleukin 1Β ◽  
No Production ◽  
Tnf Α ◽  
Ifn Γ ◽  
Cox 2 ◽  
Necrosis Factor

AbstrakRumput laut merupakan sumber daya hayati perairan yang telah diteliti mengandung sejumlah komponen bioaktif untuk meningkatkan kesehatan manusia seperti meningkatkan sistem imun atau bersifat sebagai imunomodulator.Penulisan artikel ini bertujuan untuk menjelaskan lebih jauh tentang sifat imunomodulator rumput laut, diharapkan tulisan ini dapat memberikan informasi ilmiah tentang rumput laut sebagai imunomodulator, sehingga nantinya dapat dikembangkan lagi penelitian ilmiah tentang pemanfaatan rumput laut sebagai imunomodulator.Rumput laut dapat meningkatkan sistem imun spesifik dan non spesifik melalui berbagai sel imun seperti sel makrofag, monosit atau sel limfosit melalui berbagai mekanisme di tingkat seluler.Sifat imunomodulator rumput laut dalam meningkatkan aktivasi makrofag terjadi melalui peningkatan proliferasi makrofag, produksi NO dan sekresi sitokin. Rumput laut juga dapat memodulasi aktivitas makrofag secara in vitro dan in vivo yaitu melalui ekspresi reseptor dan sitokin inflamasi seperti tumor necrosis factor (TNF-α) dan interleukin-1β (IL-1β)., produksi NO dan PGE2 dan ekspresi gen NOS-2 dan COX-2. Sifat imunomodulator rumput laut juga terjadi melalui peningkatan fungsi dan aktivitas limfosit. Ekstrak atau komponen bioaktif rumput laut dapat meningkatkan aktivasi limfosit, diantaranya menstimulasi aktivitas sel limfosit B yaitu melalui peningkatan produksi antibodi imonoglobulin (Ig), meningkatkan proliferasi sel T dan produksi subset limfosit T seperti CD4 dan CD8. Ekstrak rumput laut juga telah diteliti  mempengaruhi ekspresi mRNA untuk meningkatkan produksi  sitokin oleh Th1 seperti TNF-α dan IFN-γ, dan menurunkan sitokin yang diproduksi oleh Th2 seperti  IL-4 dan IL-10 serta  meningkatkan produksi IL-2 pada sel limfosit T.Kata kunci: rumput laut; komponen bioaktif; imunomodulatori; makrofagAbstractSeaweed is one of the marine biological resources that is known to contain bioactive compounds to improve human health, such as enhancing the immune system or being as an immunomodulator. This study aims to explain more about the nature of seaweed immunomodulators so that scientific research could be developed in the use of seaweed as an immunomodulator later. Seaweed could increase specific and nonspecific immune systems by involving various immune cells such as macrophage cells, monocytes, or lymphocyte cells through various mechanisms at the cellular level. The role of Immunomodulatory properties of seaweed in increasing macrophage activation occurs through increasing macrophage proliferation, NO production, and cytokine secretion. Seaweed would modulate macrophage activity in vitro and in vivo through the expression of inflammatory receptors and cytokines such as tumor necrosis factor (TNF-α) and interleukin-1β (IL-1β), NO and PGE2 production and NOS-gene expression 2 and COX-2. Seaweed immunomodulatory activity would also occur through increasing function and activity of lymphocytes that stimulate the activity of B lymphocyte cells, production of antibody immunoglobulin (Ig), T cell proliferation and production of T lymphocyte subsets such as CD4 and CD8. Seaweed extracts also have been investigated to be able to affect mRNA expression to increase cytokine production by Th1 such as TNF-α and IFN-γ, decrease cytokines produced by Th2 such as IL-4 and IL-10 and increase IL-2 production in T lymphocytes.Keywords: seaweed; bioactive components; immunomodulatory; macrophage 

IL-1β and TNF-α Regulate IL-6-type Cytokines in Gingival Fibroblasts

2008 ◽  
Vol 87 (6) ◽  
pp. 558-563 ◽  
Author(s):  
P. Palmqvist ◽  
P. Lundberg ◽  
I. Lundgren ◽  
L. Hänström ◽  
U.H. Lerner
Keyword(s):  
Tumor Necrosis Factor ◽  
Interleukin 6 ◽  
Leukemia Inhibitory Factor ◽  
Tumor Necrosis ◽  
Map Kinases ◽  
Tumor Necrosis Factor Receptor ◽  
Oncostatin M ◽  
Gingival Fibroblasts ◽  
Tnf Α ◽  
Necrosis Factor

Interleukin-6 (IL-6)-type cytokines are pleiotropic molecules capable of stimulating bone resorption and expressed by numerous cell types. In the present study, we tested the hypothesis that gingival fibroblasts may exert local osteotropic effects through production of IL-6 and related cytokines. IL-6-type cytokine expression and regulation by IL-1β and tumor necrosis factor-α (TNF-α) were studied in fibroblasts from the non-inflamed gingiva of healthy individuals. Constitutive mRNA expression of IL-6, IL-11, and leukemia inhibitory factor (LIF), but not of oncostatin M (OSM), was demonstrated, as was concentration-dependent stimulation of IL-6 and LIF mRNA and of protein by IL-1β and TNF-α. IL-11 mRNA and protein were concentration-dependently stimulated by IL-1β. The signaling pathway involved in IL-6 and LIF mRNA stimulation involved MAP kinases, but not NF-κB. The findings support the view that resident cells may influence the pathogenesis of periodontal disease through osteotropic IL-6-type cytokine production mediated by activation of MAP kinases. Abbreviations: IL-1α (interleukin-1α); IL-1β (interleukin-1β); IL-6 (interleukin-6); IL-11 (interleukin-11); LIF (leukemia inhibitory factor); OSM (oncostatin M); α(1)-coll. I (α(1)-collagen I); ALP (alkaline phosphatase); BMP-2 (bone morphogenetic protein-2); OC (osteocalcin); BSP (bone sialoprotein); TNFR I (tumor necrosis factor receptor I); TNFR II (tumor necrosis factor receptor II); IL-1R1 (interleukin-1 receptor 1); GAPDH (glyceraldehyde-3-phosphate dehydrogenase); RPL13A (ribosomal protein L13A); mRNA (messenger ribonucleic acid); cDNA (complementary deoxyribonucleic acid); PCR (polymerase chain-reaction); BCA (bicinchoninic acid); ELISA (enzyme-linked immunosorbent assay); α-MEM (α modification of Minimum Essential Medium); and FCS (fetal calf serum).

Epinephrine inhibits endotoxin-induced IL-1β production: roles of tumor necrosis factor-α and IL-10

1997 ◽  
Vol 273 (6) ◽  
pp. R1885-R1890 ◽  
Author(s):  
Tom Van Der Poll ◽  
Stephen F. Lowry
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Ex Vivo ◽  
Systemic Infection ◽  
Tnf Α ◽  
Cytokine Tumor Necrosis Factor ◽  
Dose Dependent Decrease ◽  
Factor Α ◽  
Necrosis Factor

Epinephrine has been found to inhibit the production of the proinflammatory cytokine tumor necrosis factor (TNF)-α and to enhance the production of anti-inflammatory cytokine interleukin (IL)-10. To determine the effect of epinephrine on IL-1β production, the following experiments were performed: 1) blood obtained from subjects at 4–21 h after the start of a continuous infusion of epinephrine (30 ng ⋅ kg−1⋅ min−1) produced less IL-1β after ex vivo stimulation with lipopolysaccharide (LPS), compared with blood drawn from subjects infused with saline; 2) in whole blood in vitro, epinephrine caused a dose-dependent decrease in LPS-induced IL-1β production, which was likely mediated via adrenergic receptors; and 3) inhibition of TNF and enhancement of IL-10 both contributed to epinephrine-induced inhibition of IL-1β production. Epinephrine, either endogenously produced or administered as a component of sepsis treatment, may attenuate excessive activity of proinflammatory cytokines early in the course of systemic infection.

scholarly journals Ectopic HOXB4 overcomes the inhibitory effect of tumor necrosis factor-α on Fanconi anemia hematopoietic stem and progenitor cells

Blood ◽  
2009 ◽  
Vol 113 (21) ◽  
pp. 5111-5120 ◽  
Author(s):  
Michael D. Milsom ◽  
Bernhard Schiedlmeier ◽  
Jeff Bailey ◽  
Mi-Ok Kim ◽  
Dandan Li ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Fanconi Anemia ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Ectopic Expression ◽  
Hematopoietic Stem ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

AbstractEctopic delivery of HOXB4 elicits the expansion of engrafting hematopoietic stem cells (HSCs). We hypothesized that inhibition of tumor necrosis factor-α (TNF-α) signaling may be central to the self-renewal signature of HOXB4. Because HSCs derived from Fanconi anemia (FA) knockout mice are hypersensitive to TNF-α, we studied Fancc−/− HSCs to determine the physiologic effects of HOXB4 on TNF-α sensitivity and the relationship of these effects to the engraftment defect of FA HSCs. Overexpression of HOXB4 reversed the in vitro hypersensitivity to TNF-α of Fancc−/− HSCs and progenitors (P) and partially rescued the engraftment defect of these cells. Coexpression of HOXB4 and the correcting FA-C protein resulted in full correction compared with wild-type (WT) HSCs. Ectopic expression of HOXB4 resulted in a reduction in both apoptosis and reactive oxygen species in Fancc−/− but not WT HSC/P. HOXB4 overexpression was also associated with a significant reduction in surface expression of TNF-α receptors on Fancc−/− HSC/P. Finally, enhanced engraftment was seen even when HOXB4 was expressed in a time-limited fashion during in vivo reconstitution. Thus, the HOXB4 engraftment signature may be related to its effects on TNF-α signaling, and this pathway may be a molecular target for timed pharmacologic manipulation of HSC during reconstitution.

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