scholarly journals Endothelin-1 stimulates human monocytes in vitro to release TNF-α , IL-1β and IL-6

1993 ◽  
Vol 2 (6) ◽  
pp. 417-422 ◽  
Author(s):  
E. Helset ◽  
T. Sildnes ◽  
R. Seljelid ◽  
Z.S. Konopski
Keyword(s):  
2001 ◽  
Vol 69 (6) ◽  
pp. 3906-3915 ◽  
Author(s):  
Winston M. Manimtim ◽  
Jeffrey D. Hasday ◽  
Lisa Hester ◽  
Karen D. Fairchild ◽  
Judith C. Lovchik ◽  
...  

ABSTRACT We previously observed that Ureaplasma urealyticumrespiratory tract colonization in infants with a birth weight of ≤1,250 g was associated with increases in the tracheal aspirate proinflammatory cytokines tumor necrosis factor alpha (TNF-α) and interleukin-8 (IL-8) relative to the counterregulatory cytokine IL-6 during the first week of life (A. M. Patterson, V. Taciak, J. Lovchik, R. E. Fox, A. B. Campbell, and R. M. Viscardi, Pediatr. Infect. Dis. J. 17:321–328, 1998). We hypothesized thatU. urealyticum alters the host immune response in the presence of a coinflammatory stimulus (e.g., bacterial infection or hyperoxia) by shifting the balance of cytokine expression towards the proinflammatory cytokines. To test this hypothesis, we compared the release of TNF-α, IL-8, IL-6, and IL-10 in vitro by unstimulated andU. urealyticum (with or without lipopolysaccharide [LPS])-stimulated human monocytes from adult peripheral blood and from term and preterm cord blood. U. urealyticum alone and in combination with LPS induced concentration- and development-dependent changes in cytokine release. In vitro inoculation with low-inoculum U. urealyticum (103color-changing units [CCU]) (i) partially blocked the LPS-stimulated IL-6 release by all cells and reduced LPS-stimulated IL-10 release by preterm cells, (ii) stimulated TNF-α and IL-8 release by preterm cells, and (iii) augmented LPS-stimulated TNF-α release in all cells. In preterm cells, high-inoculum U. urealyticum(106 CCU) (i) stimulated TNF-α and IL-8, but not IL-6 or IL-10, release and (ii) augmented LPS-stimulated TNF-α and IL-8 release. High-inoculum U. urealyticum (i) stimulated release of all four cytokines in term cells and IL-8 release in adult cells and (ii) augmented LPS-induced TNF-α, IL-10, and IL-8 release in term cells but did not significantly affect LPS-induced cytokine release in adult cells. We speculate that U. urealyticum enhances the proinflammatory response to a second infection by blocking expression of counterregulatory cytokines (IL-6 and IL-10), predisposing the preterm infant to prolonged and dysregulated inflammation, lung injury, and impaired clearance of secondary infections.


2014 ◽  
Vol 307 (11) ◽  
pp. H1547-H1558 ◽  
Author(s):  
Roddy Hiram ◽  
Edmond Rizcallah ◽  
Chantal Sirois ◽  
Marco Sirois ◽  
Caroline Morin ◽  
...  

Pulmonary hypertension (PH) is a rare and progressive disease characterized by an inflammatory status and vessel wall remodeling, resulting in increased pulmonary artery resistance. During the last decade, treatments have been proposed; most of them target the endothelial pathways that stimulate smooth muscle cell relaxation. However, PH remains associated with significant morbidity. We hypothesized that inflammation plays a crucial role in the severity of the abnormal vasoconstriction in PH. The goal of this study was to assess the effects of resolvin D1 (RvD1), a potent anti-inflammatory agent, on the pharmacological reactivity of human pulmonary arteries (HPAs) via an in vitro model of induced hyperreactivity. The effects of RvD1 and monoacylglyceride compounds were measured on contractile activity and Ca2+ sensitivity developed by HPAs that had been pretreated (or not) under proinflammatory conditions with either 10 ng/ml TNF-α or 10 ng/ml IL-6 or under hyperreactive conditions with 5 nM endothelin-1. The results demonstrated that, compared with controls, 24-h pretreatment with TNF-α, IL-6, or endothelin-1 increased reactivity and Ca2+ sensitivity of HPAs as revealed by agonist challenges with 80 mM KCl, 1 μM serotonin (5-hydroxytryptamine), 30 nM U-46619, and 1 μM phorbol 12,13-dibutyrate. However, 300 nM RvD1 as well as 1 μM monoacylglyceride-docosapentaenoic acid monoglyceride strongly reversed the overresponsiveness induced by both proinflammatory and hyperreactive treatments. In pretreated pulmonary artery smooth muscle cells, Western blot analyses revealed that RvD1 treatment decreased the phosphorylation level of CPI-17 and expression of transmembrane protein member 16A while increasing the detection of G protein-coupled receptor 32. The present data demonstrate that RvD1, a trihydroxylated docosahexaenoic acid derivative, decreases induced overreactivity in HPAs via a reduction in CPI-17 phosphorylation and transmembrane protein member 16A expression.


2013 ◽  
Vol 2013 ◽  
pp. 1-7 ◽  
Author(s):  
Marisol Pérez-Acosta ◽  
Félix Giovanni Delgado ◽  
Jaime E. Castellanos

Dengue virus (DENV) produces an acute infection that results in the overproduction of proinflammatory cytokines. Although increased levels of the immunoregulator soluble ST2 (sST2) protein have been reported in the serum of patients with dengue, its importance during DENV infection remains unclear. The purpose of this study was to evaluate the effect of a recombinant human sST2 protein on the production of TNF-α and IL-6 in an in vitro model of DENV infection. Peripheral blood mononuclear cells (PBMCs) were permissive to in vitro DENV infection since viral antigen was detected in CD14+ monocytes by flow cytometry (median, 1%; range, 0–2.2), and in their supernatants TNF-α and IL-6 were detected. However, sST2 protein was not detected. Using multiple staining on infected PBMC we found that only CD14+ cells produced TNF-α and IL-6. Treatment with human recombinant sST2 protein decreased lipopolysaccharide-induced monocyte TNF-α and IL-6 production. However, this effect was not observed when the monocytes were pretreated with sST2 and later infected with DENV-2. These results suggest that sST2 has different roles in the regulation of TNF-α and IL-6 expression in human monocytes stimulated with LPS and DENV-2.


2011 ◽  
Vol 106 (1) ◽  
pp. 33-36 ◽  
Author(s):  
Giuliana Trefiletti ◽  
Anna Rita Togna ◽  
Valentina Latina ◽  
Carolina Marra ◽  
Marcella Guiso ◽  
...  

Extra-virgin olive oil is an integral ingredient of the Mediterranean diet, and it has been suggested that its high consumption has beneficial effects on human health. Its protective effect, in particular against the development of CVD, has been related not only to the high content of oleic acid, but also to the antioxidant and anti-inflammatory properties of polyphenols. In order to verify the anti-inflammatory and anti-atherogenic properties of hydroxy-isochromans, a class of ortho-diphenols present in extra-virgin olive oil, we investigated the potential ability of 1-phenyl-6,7-dihydroxy-isochroman (L137) to modulate the production of key inflammatory mediators by human monocytes, by evaluating its in vitro effects on prostanoid (thromboxane A2 and PGE2) and cytokine (TNF-α) production. Its effect on the protein expression of the inducible form of cyclo-oxygenase-2 (COX-2), a pro-inflammatory enzyme responsible for elevated prostanoid levels, was also explored. The results showed that L137 significantly inhibited both prostanoid and TNF-α production in lipopolysaccharide-primed human monocytes in a dose-dependent manner, by inhibiting the COX activity of COX-2. We also demonstrated that the effects of the isochroman are mediated, at least partly, through the suppression of NF-κB activation leading to the down-regulation of the synthesis of COX-2.


1997 ◽  
Vol 136 (4) ◽  
pp. 542-547 ◽  
Author(s):  
U. MROWIETZ ◽  
H. JESSAT ◽  
A. SCHWARZ ◽  
T. SCHWARZ
Keyword(s):  

2009 ◽  
Vol 77 (3) ◽  
pp. 1238-1245 ◽  
Author(s):  
Vida A. Dennis ◽  
Saurabh Dixit ◽  
Shannon M. O'Brien ◽  
Xavier Alvarez ◽  
Bapi Pahar ◽  
...  

ABSTRACT We investigated the mechanisms that lead to the production of proinflammatory mediators by human monocytes when these cells are exposed in vitro to live Borrelia burgdorferi spirochetes. We first focused on myeloid differentiation primary response protein 88 (MyD88), an adapter molecule that is essential in the Toll-like receptor (TLR) pathway. Real-time PCR, flow cytometry, and confocal microscopy experiments revealed that MyD88 was maximally expressed in THP-1 cells after 24-h stimulation of these cells with live B. burgdorferi. Silencing of the MYD88 gene by using small interfering RNA resulted in 24%, 35%, and 84% down-modulation of the production of tumor necrosis factor alpha (TNF-α), interleukin-8 (IL-8), and IL-6, respectively, in THP-1 cells stimulated with live B. burgdorferi. Specific silencing of the TLR1, TLR2, or TLR5 gene by RNA interference further revealed that silencing of the TLR1 and TLR2 genes alone or combined, but not the TLR5 gene, caused a downregulation of IL-6, IL-8, and TNF-α in live B. burgdorferi-stimulated THP-1 cells. Overall, similar results were obtained for THP-1 cells stimulated with purified lipoproteins. Our results indicate that the TLR pathway mediates, at least in part, the release of inflammatory mediators in human monocytes stimulated with live B. burgdorferi spirochetes and furthermore suggest that the TLR-dependent interaction between these cells and live spirochetes is mediated by spirochetal lipoproteins but not by flagellin.


2019 ◽  
Vol 6 (2) ◽  
pp. 87-92
Author(s):  
Fiona Budi Amarta Domini ◽  
I Dewa Ayu Ratna Dewanti ◽  
Erawati Wulandari

Monocytes play a role in the first defense against microorganisms that harm the body by activating nuclear factor kβ (Nf-kβ) which is the main regulator of inflammatory genes, one of which is TNF-α. TNF-α at excessive levels will cause tissue damage. Therefore an immunomodulator is needed which can regulate the body's immune system. One natural ingredient that acts as an immunomodulator is fish bones. Purpose of research: To analyze the effect of goatfish’s bone extract on TNF-α expression in human monocytes exposed to P. gingivalis. Method: experimental laboratories in vitro. TNF-α expression was tested by imunocytochemical techniques. Results: The results showed that the average number of monocytes expressing TNF-α in group P1 (group of diclofenac sodium) was 42.33 cells per cell. In the P2 group (P. gingivalis group) was 95 cell percent cells and for P3 (fish bone group) was 74.33 cells per cell and the control group was 11.66 cells per hundred cells. Conclusion: goatfish’s bone extract can act as an anti-inflammatory which is effective in reducing TNF-α expression in monocyte exposed to P. gingivalis but less effective than diclofenac sodium.


1997 ◽  
Vol 136 (4) ◽  
pp. 542-547 ◽  
Author(s):  
U. MROWIETZ ◽  
H. JESSAT ◽  
A. SCHWARZ ◽  
T. SCHWARZ
Keyword(s):  

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