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At least 19 recordsLinked to original sources
PubMed2002

Effects of Rosa canina fruit extract on neutrophil respiratory burst.

Respiratory burst leads polymorphonuclear neutrophils (PMN) to produce reactive oxygen species (ROS) such as superoxide anions (O(2)(o-)), hypochlorous acid (HOCl) and hydrogen peroxide (H(2)O(2)) which may possess deleterious effects for the organism. Rosa canina fruits are well known to contain a large amount of vitamin C which is antioxidant. This study was focused on the polyphenolics contained in rose hips to evaluate their antioxidative properties. We prepared a rose hip extract deprived of vitamin C. The extract contained mainly phenolics such as proanthocyanidins and flavonoids. We investigated its effects directly against (O(2)(o-)), HOCl and H(2)O(2) and investigated its effects on isolated PMN. For that, in vitro inflammatory conditions were reproduced by stimulating PMN with stimuli having different transductional pathways, in order to determine a possible mechanism of action. The results showed that the extract can inhibit ROS tested in acellular and cellular systems. The IC(50) obtained were 5.73 mg/L, 1.33 mg/L and 2.34 mg/L respectively for (O(2)(o-)), HOCl and H(2)O(2) in acellular experiments. For cellular experiments, the IC(50) were quite similar. Thus, the extract did not present an effect on PMN metabolism. Therefore, the antioxidative effects of Rosa canina are due not only to vitamin C but also to polyphenolics.

Anthocyanins↗
PubMed1990

Turning on the respiratory burst.

The respiratory burst is a distinguishing property of phagocytes. It is induced by chemotactic stimulation or phagocytosis and reflects the activation of a membrane-bound enzyme system that transfers electrons from cytosolic NADPH to extracellular oxygen, producing superoxide. The products of the burst are essential for the killing of microorganisms, but are also a cause of tissue damage and inflammation. Studies aimed at a better understanding of the regulation of the respiratory burst should help in the search for new ways to treat infections and inflammation.

Animals↗
PubMed1993

Nanomolar arachidonic acid influences the respiratory burst in eosinophils and neutrophils induced by GTP-binding protein. A comparative study of the respiratory burst in bovine eosinophils and neutrophils.

To investigate a possible role of phospholipase A2 (PLA2) in the respiratory burst in bovine eosinophilic and neutrophilic leukocytes dependent on GTP-binding protein (G-protein), we permeabilized these cells with Staphylococcus aureus alpha-toxin and induced NADPH oxidase activity with the non-hydrolysable GTP analogue GTP[S] or the aluminium tetrafluoro complex AlF4-. Under same experimental conditions, cells responded with different onset times. The onset time for eosinophils was 50-200 s, for neutrophils it was only a few seconds. GTP[S] stimulated in neutrophils only 5% of the respiratory burst compared to eosinophils, whereas AlF4(-)-induced comparable responses (neutrophils 120% of eosinophils). GDP inhibited these responses with an IC50 value of 2.4 mM. Arachidonic acid showed, with the exception of AlF4- stimulated neutrophils, on both stimuli and cell types an enhancing effect (150%) that reached its maximum at 0.1-1 microM. The PLA2 inhibitor 4-bromophenacylbromide reduced the GTP[S]- and AlF4(-)-induced response almost completely (10 microM) and the inhibition was not significantly different for eosinophils and neutrophils (IC50 1-3 microM). If the respiratory burst was reduced with 4-bromophenacylbromide to 1-4% of the original value, 10% of the basal NADPH oxidase activity could be restored by addition of only 20-100 nM arachidonic acid. In addition, the PLA2 activator adriamycin enhanced the response in a dose-dependent manner and in the same order as arachidonic acid did. The results presented above suggest that the respiratory burst may be regulated by different low-molecular-mass and/or heterotrimeric G-proteins and an active role for arachidonic acid or its metabolites in the activation and the maintenance of the direct G-protein-stimulated respiratory burst in bovine eosinophils and neutrophils.

Aluminum Compounds↗
PubMed1994

Rat brain microglia and peritoneal macrophages show similar responses to respiratory burst stimulants.

Respiratory burst activity was compared between cultured newborn rat microglia and directly harvested adult rat peritoneal macrophages using a Clarke oxygen electrode system. Both types of cells showed stimulated oxygen consumption almost immediately after the administration of opsonized zymosan, phorbol myristate acetate, concanavalin A, or tuftsin. The absolute values of stimulated oxygen consumption after administration of these agents ranged from 0.11 to 0.99 nmol per min per million cells, with some variation in relative response of microglia compared with peritoneal macrophages. After lysis of cells with deoxycholate, or disruption by sonication, oxygen consumption was restored by NADPH for stimulated microglia but not stimulated astrocytes. The potential for stimulated microglia to generate oxygen free radicals may have implications in several degenerative neurological diseases where activated microglia are found in association with the lesions.

Animals↗
PubMed1997

Acute regulation of glucose transport in a monocyte-macrophage cell line: Glut-3 affinity for glucose is enhanced during the respiratory burst.

Activation of the respiratory burst imposes acute metabolic demands on phagocytic cells. These are met by mobilizing internal energy stores and by increasing the utilization of exogenous energy, including glucose in the circulation. To determine whether the increased glucose uptake that is known to be associated with the respiratory burst involves the regulation of glucose transporter molecules, the intrinsic transport properties of glucose transporters on the macrophage cell line RAW 264.7 were determined after activation with PMA, N-formyl-methionine-leucine-phenylalanine (fMLP) and the cytokines granulocyte/macrophage colony-stimulating factor (GM-CSF) and interleukin 3 (IL-3). Treatment with PMA resulted in a 2-fold increase in respiratory burst activity within 10 min; this was associated with a 30-50% increase in 2-deoxyglucose uptake and a 4-fold increase in transporter affinity for glucose. Similarly, fMLP, GM-CSF and IL-3 treatments stimulated 2-deoxyglucose uptake that was associated with a 3-4-fold increase in transporter affinity for glucose. To determine whether the changes observed in 2-deoxyglucose uptake in response to PMA, fMLP and growth factors were influenced by phosphorylation of the sugar, 3-O-methylglucose, which is not phosphorylated, was used. Increased 3-O-methylglucose uptake and increased transporter affinity for glucose were also observed after PMA, fMLP and GM-CSF treatments. Whereas both fMLP and GM-CSF stimulated superoxide production, IL-3 failed to activate respiratory burst activity. The protein kinase inhibitors genistein and staurosporine inhibited the increase in 2-deoxyglucose uptake observed with fMLP and GM-CSF, and partly reversed the affinity increase towards that of untreated control cells. In contrast, the phosphatidylinositol 3-kinase inhibitor wortmannin had little effect on 2-deoxyglucose uptake in response to these activators. Western blotting with subtype-specific antisera showed that Glut-3 was the predominant transporter on RAW 264.7 cells. These studies demonstrate that acute regulation of glucose transporters occurs in response to activators that promote respiratory burst activity, and show that this regulation involves both tyrosine kinases and protein kinase C activity.

3-O-Methylglucose↗
PubMed1986

Progressive loss of the macrophage respiratory burst in oxygen toxicity.

The respiratory burst of rat alveolar macrophages stimulated by a variety of agents declines as a function of time of exposure to hyperoxia. Previous studies have evaluated this effect in terms of the stimulated O(2) production of a population of cells. The present study was designed to determine whether this decline is due to a "turning off" of the respiratory burst activity of some cells within the alveolar macrophage population or a general suppression of the activity of all cells. The phorbol myristate acetate (PMA) initiated respiratory burst of individual rat alveolar macrophages was monitored using the reaction of nitroblue tetrazolium (NBT), which results in the formation of a precipitate on active cells. The formazan staining was evaluated using black and white photographs of the cells and comparison to a scale constructed from photographed cells of four differing intensities of staining. Frequency distributions indicated that when the respiratory burst capability in the population of alveolar macrophages is impaired approximately 50% by oxygen exposure and/or culture in plastic vessels with artificial media, there is a gradual shift in NBT reduction rather than an "all or nothing" mechanism, in which the distribution would have reflected a shift from darkly stained cells to the very lessened or negligible staining observed at the end stage of oxygen toxicity.

Animals↗
PubMed2000

Regulatory role of extracellular matrix proteins in neutrophil respiratory burst during aging.

Neutrophil respiratory burst was assessed on plates coated with fibronectin (FN) or laminin (LM), both used at dosages inhibiting polystyrene-triggered cell activation in young healthy volunteers. Under these conditions, a low, yet significant, spontaneous superoxide anion (O(2)(-)) production, matching with enhanced levels of basal adherence, was detected in FN-plated neutrophils of elderly donors. In contrast, although neutrophil stimulation with tumor necrosis factor (TNF)-alpha, granulocyte macrophage-colony stimulating factor (GM-CSF), fMLP or phorbol myristate acetate (PMA) gave rise to a massive and prolonged FN-primed O(2)(-) release, a significant impairment of oxidative response occurred in the aged group as a result of GM-CSF or fMLP cell challenge. Such an effect was not associated to an age-related imbalance of stimulant-triggered neutrophil adhesiveness to FN, even though a larger contribution of CD18-dependent versus CD18-independent pathways was observed in old as compared to young individuals. Notably, within the aged group, anti-CD18 monoclonal antibody cell pretreatment resulted in a higher suppression of FN-primed O(2)(-) release following TNF-alpha with respect to GM-CSF stimulation, thus implying that an agonist-related defect of the coupling between beta2 integrin-dependent adhesive and oxidative events is likely to occur as a feature of age. All physiological mediators failed to activate the respiratory burst of neutrophils plated on LM-coated wells in both young and aged donors. This effect appears to be the result of an active process, since neutrophils from either group of subjects adhered to LM-coated surfaces and LM inhibited in a dose-dependent manner the FN-priming effect on neutrophil O(2)(-) production. All together the findings provide additional evidence for an imbalance of neutrophil-mediated functions in the elderly.

Aged↗
PubMedDate not supplied

In vitro studies on the regulation of rainbow trout (Oncorhynchus mykiss) macrophage respiratory burst activity.

Modulation of the respiratory burst activity of head kidney macrophages isolated from rainbow trout (Oncorhynchus mykiss) was observed following treatment with several biologically active substances. Macrophage-activating factor (MAF) induced the highest increment if respiratory burst activity relative to treatment with lipopolysaccharide (LPS), tumor necrosis factor alpha (TNF alpha) or beta-glucans from Saccharomyces cerevisiae. Increased responses were more evident when these molecules were combined in pairs. Negative regulation of respiratory burst activity was observed when diMePGE2 was added to the macrophages, with maximal inhibition seen using a concentration of 2.6 microM. Inhibition was also seen using stimulated macrophages, either by co-incubation of stimuli and diMePGE2 or by adding diMePGE2 to previously stimulated cells. The inhibitory effect on macrophages was detectable with 3 h of incubation with diMePGE2 and by 24 h the level of the response was even lower than that from unstimulated (control) macrophages. Of significance was the finding that the inhibitory effect of prostaglandin on macrophage function could be overcome by co-incubation with stimulatory molecules or by pre-treatment with MAF and LPS or MAF and TNF alpha Thus, the regulation of macrophage activation in fish is likely to be as complex as in mammals.

16,16-Dimethylprostaglandin E2↗
PubMed2003

Akt phosphorylates p47phox and mediates respiratory burst activity in human neutrophils.

Respiratory burst activity and phosphorylation of an NADPH oxidase component, p47(phox), during neutrophil stimulation are mediated by phosphatidylinositol 3-kinase (PI-3K) activation. Products of PI-3K activate several kinases, including the serine/threonine kinase Akt. The present study examined the ability of Akt to regulate neutrophil respiratory burst activity and to interact with and phosphorylate p47(phox). Inhibition of Akt activity in human neutrophils by an inhibitory peptide significantly attenuated fMLP-stimulated, but not PMA-stimulated, superoxide release. Akt inhibitory peptide also inhibited hydrogen peroxide generation stimulated by bacterial phagocytosis. A direct interaction between p47(phox) and Akt was shown by the ability of GST-p47(phox) to precipitate recombinant Akt and to precipitate Akt from neutrophil lysates. Active recombinant Akt phosphorylated recombinant p47(phox) in vitro, as shown by (32)P incorporation, by a mobility shift change detected by two-dimensional gel electrophoresis, and by immunoblotting with phospho-Akt substrate Ab. Mutation analysis indicated that 2 aa residues, Ser(304) and Ser(328), were phosphorylated by Akt. Inhibition of Akt activity also inhibited fMLP-stimulated neutrophil chemotaxis. We propose that Akt mediates PI-3K-dependent p47(phox) phosphorylation, which contributes to respiratory burst activity in human neutrophils.

Androstadienes↗
PubMed1995

The respiratory burst oxidase.

The respiratory burst oxidase catalyzes the production of O2- by activated phagocytes and B lymphocytes. Activation is accomplished by any number of signal transduction pathways, and involves protein kinase C, MAP kinase, or both, and perhaps lipid-mediated pathways. Failure of O2- production is characteristic of chronic granulomatous disease, an inherited disorder of phagocyte function. A number of new mutations responsible for chronic granulomatous disease have been reported. O2- production is also altered in other diseases, most notably certain hematologic malignancies.

Enzyme Activation↗
PubMed1994

Activation of the respiratory burst oxidase.

The respiratory burst oxidase of phagocytes and B lymphocytes catalyzes the reduction of oxygen by NADPH to form O2-, the precursor of a group of reactive oxidants that are employed by phagocytes as microbicidal agents. The enzyme is active in stimulated cells but dominant in resting cells. It molecular weight guanine nucleotide-binding protein. The components p22phox and gp91phox from cytochrome b558, a flavohemoprotein that resides in the cortical cytoskeleton and in the membranes of the specific granules. The other components are found in the cytosol of resting cells, but migrate to the cortical cytoskeleton when the neutrophils are activated, where they assemble the active oxidase. Migration to the cortical cytoskeleton is caused in part by the appearance of a membrane binding site on one or more of the cytosolic subunits, possibly due to the phosphorylation of p47phox that takes place during cell activation.

B-Lymphocytes↗
PubMed1991

Identification of the NADPH-binding subunit of the respiratory burst oxidase.

The respiratory burst oxidase is a multicomponent membrane-bound enzyme that uses NADPH to reduce oxygen to O2-. When oxidase-containing membranes from activated neutrophils are treated with 0.3 M KCl, the NADPH-binding component of the oxidase elutes from the membranes in an active form. Treatment of this eluate with [32P]NADPH dialdehyde labels an approximately 32-kDa protein that is absent from eluates obtained from normal resting membranes or from resting or activated membranes from patients with one form of chronic granulomatous disease. We propose that this approximately 32-kDa protein is the NADPH-binding component of the oxidase.

Cell Membrane↗
PubMed1988

The respiratory burst oxidase.

The respiratory burst oxidase is an activatable, membrane-bound flavo(?hemo) protein that catalyzes the NADPH-dependent reduction of oxygen to superoxide (O2-) in stimulated phagocytes. Chronic granulomatous disease, a group of disorders in which phagocytes cannot manufacture O2-, is caused by a biochemical lesion involving this oxidase or its activating system.

Cytochrome b Group↗
PubMed1985

Respiratory bursts at the midline of the rostral medulla of the lamprey.

The contribution of a rostral crossed pathway to the coordination of fictive breathing was tested in isolated brains of adult lampreys, Ichthyomyzon unicuspis. Periodic bursts of small spikes were recorded at the midline at the rostral level of the V motor nuclei. These occurred prior to bursts by respiratory motoneurons in the IX-X cranial nerve roots. The bursts at the midline could be generated in the rostral half of the medulla, since they continued after isolation of the isthmic-trigeminal region by transections. Stimulation at the rostral midline excited respiratory motoneurons monosynaptically and could entrain or reset the respiratory rhythm. Sections of the midline sparing the rostral site still permitted bilateral synchronization of respiratory bursts. Alternatively, sections of the rostral midline still allowed coordination of respiratory bursts through crossed caudal pathways, although abnormal timing patterns were observed. It is concluded that the motor pattern for respiration is partly generated and coordinated in the rostral half of the medulla of the lamprey and is transmitted to respiratory motoneurons through descending pathways.

Animals↗
PubMed1997

Ca(2+)-dependent p47phox translocation in hydroperoxide modulation of the alveolar macrophage respiratory burst.

Oxidative stress produces dual effects on the respiratory burst of rat alveolar macrophages. Preincubation with hydroperoxide concentrations [H2O2 or tert-butyl hydroperoxide (t-BOOH); < 50 microM] enhances stimulation of the respiratory burst, whereas higher concentrations inhibit stimulation. Both the enhancement and inhibition are markedly attenuated by buffering t-BOOH-induced changes in intracellular Ca2+ concentration ([Ca2+]i). Phosphorylation of the NADPH oxidase component p47phox and its translocation from cytoplasm to plasma membrane are essential in respiratory burst activation. Phorbol 12-myristate 13-acetate (PMA)-stimulated p47phox phosphorylation was negligibly affected by 25 or 100 microM t-BOOH. Nonetheless, 25 microM t-BOOH increased PMA-stimulated p47phox translocation, whereas 100 microM t-BOOH decreased PMA-stimulated translocation. In unstimulated cells, however, neither phosphorylation nor translocation of p47phox was affected by t-BOOH. Buffering of the t-BOOH-mediated changes of [Ca2+]i abolished the effects of t-BOOH on PMA-stimulated translocation in parallel to effects upon the respiratory burst. The results suggest that the dual effects of hydroperoxides are mediated, in part, by Ca(2+)-dependent processes affecting the assembly of the respiratory burst oxidase at steps that are separate from p47phox phosphorylation.

Animals↗
PubMed1994

Essential role of YopD in inhibition of the respiratory burst of macrophages by Yersinia enterocolitica.

The respiratory burst is a key element of the bactericidal armamentarium of phagocytes. In this study we have shown that a virulent strain of Yersinia enterocolitica serogroup O:9 completely inhibited the ability of murine bone marrow-derived macrophages to mount a respiratory burst in response to stimulation by zymosan. This property of the bacterium was abrogated by curing the strain of its 71.5-kb virulence plasmid and by transposon mutagenesis of the plasmid-borne yopD gene. Derivatives of the bacterium which were unable to inhibit the respiratory burst were also less able to disrupt cytoskeletal actin and to resist phagocytosis. yopD mutants also showed an impaired ability to dephosphorylate phosphotyrosine residues in macrophage proteins and were completely avirulent for mice. All of these defects were fully or partly restored by trans-complementation of a yopD mutant with a cloned yopD gene. The results of this study and those of previous work with YopD (R. Rosqvist, A. Forsberg, and H. Wolf-Watz, Infect. Immun. 59:4562-4569, 1991) suggest that YopD functions chiefly by facilitating the transport of virulence plasmid-encoded proteins, such as YopE, a cytotoxin, and YopH, a protein tyrosine phosphatase, across the cytoplasmic membrane to their targets within host cells. The combined action of these Yops on cytoplasmic proteins, especially actin, could explain the effects of virulent Y. enterocolitica on macrophage morphology, phagocytic capacity, and respiratory burst activity, all of which rely on cytoskeletal integrity to function normally.

Animals↗
PubMed2001

The effect of lidocaine on neutrophil respiratory burst during induction of general anaesthesia and tracheal intubation.

BACKGROUND AND OBJECTIVE: Respiratory burst is an essential component of the neutrophil's biocidal function. In vitro, sodium thiopental, isoflurane and lidocaine each inhibit neutrophil respiratory burst. The objectives of this study were (a) to determine the effect of a standard clinical induction/tracheal intubation sequence on neutrophil respiratory burst and (b) to determine the effect of intravenous lidocaine administration during induction of anaesthesia on neutrophil respiratory burst. METHODS: Twenty ASA I and II patients, aged 18-60 years, undergoing elective surgery were studied. After induction of anaesthesia [fentanyl (2 microg kg-1), thiopental (4-6 mg kg-1), isoflurane (end-tidal concentration 0.5-1.5%) in nitrous oxide (66%) and oxygen], patients randomly received either lidocaine 1.5 mg kg-1 (group L) or 0.9% saline (group S) prior to tracheal intubation. Neutrophil respiratory burst was measured immediately prior to induction of anaesthesia, immediately before and 1 and 5 min after lidocaine/saline. RESULTS: Neutrophil respiratory burst decreased significantly after induction of anaesthesia in both groups [87.4 +/- 8.2% (group L) and 88.5 +/- 13.4% (group S) of preinduction level (P < 0.01 both groups)]. After intravenous lidocaine (but not saline) administration, neutrophil respiratory burst returned towards preinduction levels, both before (97.1 +/- 23.6%) and after (94.4 +/- 16.6%) tracheal intubation. CONCLUSION: Induction of anaesthesia and tracheal intubation using thiopentone and isoflurane, inhibit neutrophil respiratory burst. This effect may be diminished by the administration of lidocaine.

Adolescent↗