scholarly journals Ex Vivo Study on the Antioxidant Activity of a Winemaking By-Product Polyphenolic Extract (Taurisolo®) on Human Neutrophils

Antioxidants ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1009
Author(s):  
Giuseppe Annunziata ◽  
Xavier Capó ◽  
Maria Magdalena Quetglas-Llabrés ◽  
Margalida Monserrat-Mesquida ◽  
Silvia Tejada ◽  
...  
Keyword(s):  
Antioxidant Activity ◽  
Therapeutic Potential ◽  
Ex Vivo ◽  
Grape Pomace ◽  
Human Neutrophils ◽  
Necrosis Factor Alpha ◽  
Polyphenolic Extract ◽  
Nuclear Factors ◽  
Factor Alpha

Oxidative stress (OxS) has been linked to several chronic diseases and is recognized to have both major causes and consequences. The use of antioxidant-based nutraceuticals has been licensed as an optimal tool for management of OxS-related diseases. Currently, great interest is focused on the valorization of agri-food by-products as a source of bioactive compounds, including polyphenols. In this sense, we evaluated the efficacy of a novel nutraceutical formulation based on polyphenolic extract from Aglianico cultivar grape pomace (registered as Taurisolo®). In particular, we tested both native and in vitro gastrointestinal digested forms. The two extracts have been used to treat ex vivo neutrophils from subjects with metabolic syndrome, reporting a marked antioxidant activity of Taurisolo®, as shown by its ability to significantly reduce both the levels of reactive oxygen species (ROS) and the activities of catalase and myeloperoxidase in the cell medium after stimulation of neutrophils with phorbol 12-myristate 13-acetate (PMA). Interestingly, we observed an increase in intracellular enzymatic activities in PMA-treated cells, suggesting that Taurisolo® polyphenols might be able to activate nuclear factors, up-regulating the expression of this target antioxidant gene. In addition, Taurisolo® reversed the increase in malondialdehyde induced by PMA; reduced the expression of pro-inflammatory genes such as cyclooxygenase 2 (COX-2), tumor necrosis factor alpha (TNFα) and myeloperoxidase (MPO); and induced the expression of the anti-inflammatory cytokine IL-10. Overall, these results suggest the efficacy of Taurisolo® in contrasting the OxS at blood level, providing evidence for its therapeutic potential in the management of OxS-related pathological conditions in humans.

scholarly journals Erythromycin Inhibits Tumor Necrosis Factor Alpha and Interleukin 6 Production Induced by Heat-Killed Streptococcus pneumoniae in Whole Blood

1998 ◽  
Vol 42 (7) ◽  
pp. 1605-1609 ◽  
Author(s):  
Marc J. Schultz ◽  
Peter Speelman ◽  
Sebastian Zaat ◽  
Sander J. H. van Deventer ◽  
Tom van der Poll
Keyword(s):  
Streptococcus Pneumoniae ◽  
Tumor Necrosis Factor ◽  
Whole Blood ◽  
Tumor Necrosis ◽  
Cytokine Production ◽  
Ex Vivo ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Necrosis Factor

ABSTRACT To determine the effects of penicillin and erythromycin on cytokine production induced by heat-killed Streptococcus pneumoniae (HKSP), we studied the effects of those drugs on cytokine production induced by S. pneumoniaein human whole blood in vitro and ex vivo. In whole blood in vitro, erythromycin, but not penicillin, caused a dose-dependent decrease in HKSP-induced production of tumor necrosis factor alpha (TNF) and interleukin 6 (IL-6), while the production of IL-10, IL-12, and gamma interferon was inhibited only at the highest erythromycin concentration tested (10−3 M). The production of TNF and IL-6 in whole blood obtained from healthy subjects after a 30-min infusion of erythromycin (1,000 mg) was lower after ex vivo stimulation with HKSP than that in blood drawn before the infusion. Inhibition of TNF contributed to erythromycin-induced inhibition of IL-6 synthesis. Inhibition of TNF and IL-6 production by erythromycin may have a negative impact on host defense mechanisms during pneumococcal pneumonia.

scholarly journals Activation of Triggering Receptor Expressed on Myeloid Cells-1 on Human Neutrophils by Marburg and Ebola Viruses

2006 ◽  
Vol 80 (14) ◽  
pp. 7235-7244 ◽  
Author(s):  
Mansour Mohamadzadeh ◽  
Sadie S. Coberley ◽  
Gene G. Olinger ◽  
Warren V. Kalina ◽  
Gordon Ruthel ◽  
...  
Keyword(s):  
Ebola Virus ◽  
Inflammatory Responses ◽  
Myeloid Cells ◽  
Marburg Virus ◽  
Human Neutrophils ◽  
Necrosis Factor Alpha ◽  
Hemorrhagic Fevers ◽  
Factor Alpha ◽  
Necrosis Factor

ABSTRACT Marburg virus (MARV) and Ebola virus (EBOV), members of the viral family Filoviridae, cause fatal hemorrhagic fevers in humans and nonhuman primates. High viral burden is coincident with inadequate adaptive immune responses and robust inflammatory responses, and virus-mediated dysregulation of early host defenses has been proposed. Recently, a novel class of innate receptors called the triggering receptors expressed in myeloid cells (TREM) has been discovered and shown to play an important role in innate inflammatory responses and sepsis. Here, we report that MARV and EBOV activate TREM-1 on human neutrophils, resulting in DAP12 phosphorylation, TREM-1 shedding, mobilization of intracellular calcium, secretion of proinflammatory cytokines, and phenotypic changes. A peptide specific to TREM-1 diminished the release of tumor necrosis factor alpha by filovirus-activated human neutrophils in vitro, and a soluble recombinant TREM-1 competitively inhibited the loss of cell surface TREM-1 that otherwise occurred on neutrophils exposed to filoviruses. These data imply direct activation of TREM-1 by filoviruses and also indicate that neutrophils may play a prominent role in the immune and inflammatory responses to filovirus infections.

Bactericidal/permeability-increasing protein ameliorates acute lung injury in porcine endotoxemia

1994 ◽  
Vol 76 (5) ◽  
pp. 2006-2014 ◽  
Author(s):  
T. J. Vandermeer ◽  
M. J. Menconi ◽  
B. P. O′Sullivan ◽  
V. A. Larkin ◽  
H. Wang ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Human Neutrophils ◽  
Cationic Protein ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
To Receive ◽  
Necrosis Factor

Bactericidal/permeability-increasing protein (BPI), a cationic protein isolated from human neutrophils, binds lipopolysaccharide (LPS), kills gram-negative bacteria, and neutralizes many of the effects of LPS in vitro and in vivo. We hypothesized that a recombinant 23-kDa NH2-terminal fragment of BPI (BPI23) would reduce acute lung injury in endotoxemic pigs. At -18 h, pigs received an intravenous priming dose of LPS (20 micrograms/kg). Anesthetized ventilated swine were randomized to receive 1) no further treatment (n = 4); 2) LPS (250 micrograms/kg over 50 min) and BPI23 (3-mg/kg bolus and 3 mg/kg over 60 min) (n = 6); or 3) LPS and thaumatin, a cationic protein devoid of LPS neutralizing activity that has a molecular mass and isoelectric point that are similar to that of BPI23 (n = 7). BPI23 treatment significantly ameliorated LPS-induced hypoxemia, functional upregulation of opsonin receptors on circulating phagocytes, and alveolitis but had no effect on the elaboration of tumor necrosis factor-alpha or thromboxane A2. The salutory effects of BPI23 on acute lung injury in endotoxemic pigs may be mediated, at least in part, by inhibition of direct activation of phagocytes by LPS.

scholarly journals Human neutrophils produce high levels of the interleukin 1 receptor antagonist in response to granulocyte/macrophage colony-stimulating factor and tumor necrosis factor alpha.

1992 ◽  
Vol 176 (2) ◽  
pp. 593-598 ◽  
Author(s):  
S R McColl ◽  
R Paquin ◽  
C Ménard ◽  
A D Beaulieu
Keyword(s):  
De Novo ◽  
Interleukin 1 ◽  
Tnf Alpha ◽  
Human Neutrophils ◽  
Necrosis Factor Alpha ◽  
Gm Csf ◽  
Factor Alpha ◽  
Macrophage Colony

Neutrophils, an abundant cell type at sites of inflammation, have the ability to produce a number of cytokines, including interleukin 1 (IL-1), IL-8, granulocyte-macrophage colony-stimulating factor (GM-CSF), and tumor necrosis factor alpha (TNF-alpha). In this study, we have examined the ability of human neutrophils to produce the IL-1 receptor antagonist (IL-1Ra), a 17-23-kD protein recently isolated and cloned from macrophages. Since IL-1Ra has been shown to inhibit both the in vitro and in vivo effects of IL-1, its production by large numbers of tissue-invading neutrophils might provide a mechanism by which the effects of IL-1 are regulated in inflammation. Using antibodies that are specific for IL-1Ra and a cDNA probe encoding for this protein, we were able to show that neutrophils constitutively produce IL-1Ra. However, after activation by GM-CSF and TNF-alpha, IL-1Ra was secreted into the extracellular milieu where it constituted the major de novo synthesized product of activated neutrophils. None of a large array of other potent neutrophil agonists were found to affect the production of IL-1Ra by neutrophils. Quantitative measurements by enzyme-linked immunosorbent assay revealed that intracellular IL-1Ra is in eightfold excess of the amount secreted in supernatants when studying nonactivated neutrophils. However, in GM-CSF- and TNF-alpha-activated cells, this difference was reduced to values between four- and fivefold, as virtually all of the de novo synthesized IL-1Ra was secreted. In activated cells, the intracellular content of IL-1Ra was found to be in the 2-2.5-ng/ml range per 10(6) neutrophils, whereas levels reached the 0.5-ng/ml range in supernatants. This would imply that IL-1Ra is produced in excess of IL-1 by a factor of at least 100, an observation that is in agreement with the reported amounts of IL-1Ra needed to inhibit the proinflammatory effects of IL-1. Neutrophils isolated from an inflammatory milieu, the synovial fluid of patients with rheumatoid arthritis, were found to respond to GM-CSF and TNF-alpha in terms of IL-1Ra synthesis, indicating that the in vitro observations made in this study are likely to occur in an inflammatory setting in vivo.

scholarly journals Tumor Necrosis Factor Alpha Stimulates Killing of Mycobacterium tuberculosis by Human Neutrophils

2002 ◽  
Vol 70 (8) ◽  
pp. 4591-4599 ◽  
Author(s):  
Kevin O. Kisich ◽  
Michael Higgins ◽  
Gill Diamond ◽  
Leonid Heifets
Keyword(s):  
Mycobacterium Tuberculosis ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Human Neutrophils ◽  
Necrosis Factor Alpha ◽  
Reactive Nitrogen Intermediates ◽  
Factor Alpha ◽  
Necrosis Factor

ABSTRACT The ability of human neutrophils to aid in defense against pulmonary infection with Mycobacterium tuberculosis is controversial. In this study, we have shown that neutrophils respond to and phagocytose M. tuberculosis in human lesions. Neutrophils from healthy individuals were able to kill significant fractions of an inoculum of M. tuberculosis within 1 h of phagocytosis, and this ability was enhanced by tumor necrosis factor alpha but not by gamma interferon. The mycobactericidal mechanism was nonoxidative, as inhibitors of reactive oxygen or reactive nitrogen intermediates did not interfere with killing. However, the mycobactericidal mechanism was associated with increased exposure of intracellular M. tuberculosis to neutrophil defensins. In vitro, human neutrophil peptides 1 to 3 were not able to kill the bacilli even at much higher levels. These studies support the concept that human neutrophils are directly involved in defense against infection with M. tuberculosis.

Interleukin-6 Levels Decrease in Effluent from Patients Dialyzed with Bicarbonate/Lactate–Based Peritoneal Dialysis Solutions

2001 ◽  
Vol 21 (3_suppl) ◽  
pp. 102-107 ◽  
Author(s):  
Laurinda A. Cooker ◽  
Patricia Luneburg ◽  
Clifford J. Holmes ◽  
Suzanne Jones ◽  
Nicholas Topley ◽  
...  
Keyword(s):  
Peritoneal Dialysis ◽  
Interleukin 6 ◽  
Degradation Products ◽  
Ex Vivo ◽  
Buffer System ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Endothelial Growth Factor ◽  
Over Time

♦ Objective Conventional lactate-buffered peritoneal dialysis (PD) solutions have several bioincompatible characteristics, including acidic pH, lactate buffer, and the presence of glucose degradation products (GDPs). These characteristics, along with inflammation, are believed to contribute to membrane dysfunction in peritoneal dialysis patients. A new PD solution containing a bicarbonate/ lactate buffer system with physiologic pH and low GDPs has shown improved biocompatibility in both in vitro and ex vivo studies. In the present study, the concentrations of cytokines interleukin-6 (IL-6), tumor necrosis factor alpha (TNFα), and vascular endothelial growth factor (VEGF), were measured in timed overnight effluents from PD patients continuously dialyzed with either lactate-based control solution (C) or bicarbonate/lactate–based solution (B/L) for 6 months. ♦ Methods Effluents from 92 continuous ambulatory peritoneal dialysis (CAPD) patients were collected when the patients were entered into the study (baseline, all patients on C for more than 3 months), and at 3 and 6 months following randomization to C ( n = 31) or to B/L ( n = 61). Effluent samples were filtered, stored frozen, and then assayed for IL-6, TNFα, and VEGF by ELISA. ♦ Results A significant decrease in effluent IL-6 was seen at 3 months and at 6 months in the B/L-treated patients. Levels of VEGF were significantly reduced at 3 months. No changes in the levels of IL-6 or VEGF were seen in the C-treated patients, and no changes in TNFα were seen in either group over time. ♦ Conclusions Treatment with B/L is associated with decreased IL-6 synthesis and decreased VEGF secretion. The data suggest that the use of B/L solution is associated with reduced intraperitoneal inflammation and potential for angiogenesis. The use of B/L solution may, over time, help to restore peritoneal homeostasis and therefore preserve the function of the membrane in peritoneal dialysis.

Antioxidant Activity, Phenolic Content and Hematoprotective Effects of Cleome arabica Polyphenolic Leaf Extract

2019 ◽  
Author(s):  
C. Tigrine ◽  
A. Kameli
Keyword(s):  
Antioxidant Activity ◽  
Biological Effects ◽  
Reducing Power ◽  
Hematological Toxicity ◽  
Protective Effects ◽  
Ferrous Ions ◽  
Polyphenolic Extract ◽  
Cleome Arabica

In this study a polyphenolic extract from Cleome arabica leaves (CALE) was investigated for its antioxidant activity in vitro using DPPH•, metal chelating and reducing power methods and for its protective effects against AraC-induced hematological toxicity in vivo using Balb C mice. Results indicated that CALE exhibited a strong and dose-dependent scavenging activity against the DPPH• free radical (IC50 = 4.88 μg/ml) and a high reducing power activity (EC50 = 4.85 μg/ml). Furthermore, it showed a good chelating effects against ferrous ions (IC50 = 377.75 μg/ml). The analysis of blood showed that subcutaneous injection of AraC (50 mg/kg) to mice during three consecutive days caused a significant myelosupression (P < 0.05). The combination of CALE and AraC protected blood cells from a veritable toxicity. Where, the number of the red cells, the amount of hemoglobin and the percentage of the hematocrite were significantly high. On the other hand, AraC cause an elevation of body temperature (39 °C) in mice. However, the temperature of the group treated with CALE and AraC remained normal and did not exceed 37.5 °C. The observed biological effects of CALE, in vitro as well as in vivo, could be due to the high polyphenol and flavonoid contents. In addition, the antioxidant activity of CALE suggested to be responsible for its hematoprotective effect.

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