Mechanisms of Lipopolysaccharide Priming for Enhanced Respiratory Burst Activity in Human Neutrophils

Forehand, J R; Bomalski, J. S.; Johnston, Richard B.

doi:10.1007/978-1-4899-3629-5_6

Cited by 11 publications

(5 citation statements)

References 29 publications

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“…When the priming concentration of LPS was increased to 20 ng/ml, the 14.5 M lyso-PC dose activated the NADPH oxidase. Moreover, this concentration of LPS also caused significant priming of the fMLP-activated respiratory burst compared with buffer-and 2 ng/ml LPS-primed PMNs, similar to previous reports (20)(21)(22)30). At 200 ng/ml LPS, lyso-PC concentrations of 4.5 and 14.5 M activated the NADPH oxidase; furthermore, at 2 g/ml LPS, all concentrations of lyso-PCs (0.45-14.5 M) caused oxidase activation.…”

Section: Priming and Activation Of The Pmn Oxidasesupporting

confidence: 90%

“…Neutrophils are primed by a wide variety of stimulants that may be encountered during an inflammatory response (1,2,15,16,30,49,71,80,88). Exposure to small concentrations of bacterial endotoxin (lipopolysaccharide, LPS) is known to prime the respiratory burst and to augment, but not cause, elastase release from isolated PMNs (20)(21)(22)30). Priming is defined operationally on the PMN NADPH oxidase such that agents that augment the oxidative burst to a subsequent stimulus but do not individually cause oxidase assembly are termed priming agents (1,2,15,16,30,49,71,80,88).…”

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confidence: 99%

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A two-insult in vitro model of PMN-mediated pulmonary endothelial damage: requirements for adherence and chemokine release

Wyman

Bjornsen

Elzi³

et al. 2002

American Journal of Physiology-Cell Physiology

134

198

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Lysophosphatidylcholines (lyso-PCs), generated during blood storage, are etiologic in a two-insult, sepsis-based model of transfusion-related acute lung injury (TRALI). Individually, endotoxin (LPS) and lyso-PCs prime but do not activate neutrophils (PMNs). We hypothesized that priming of PMNs alters their reactivity such that a second priming agent causes PMN activation and endothelial cell damage. PMNs were primed or not with LPS and then treated with lyso-PCs, and oxidase activation and elastase release were measured. For coculture experiments, activation of human pulmonary microvascular endothelial cells (HMVECs) was assessed by ICAM-1 expression and chemokine release. HMVECs were stimulated or not with LPS, PMNs were added, cells were incubated with lyso-PCs, and the number of viable HMVECs was counted. Lyso-PCs activated LPS-primed PMNs. HMVEC activation resulted in increased ICAM-1 and release of ENA-78, GRO alpha, and IL-8. PMN-mediated HMVEC damage was dependent on LPS activation of HMVECs, chemokine release, PMN adhesion, and lyso-PC activation of the oxidase. In conclusion, sequential exposure of PMNs to priming agents activates the microbicidal arsenal, and PMN-mediated HMVEC damage was the result of two insults: HMVEC activation and PMN oxidase assembly.

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Section: Priming and Activation Of The Pmn Oxidasesupporting

confidence: 90%

mentioning

confidence: 99%

A two-insult in vitro model of PMN-mediated pulmonary endothelial damage: requirements for adherence and chemokine release

Wyman

Bjornsen

Elzi³

et al. 2002

American Journal of Physiology-Cell Physiology

134

198

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“…An increased priming response can reflect an increased susceptibility to priming or to increased amounts of substances with a priming effect. Such substances may originate from the host, e.g., proinflammatory cytokines and degradation products (Wachtfogel et al 1988, Steinbeck & Roth 1989 or from bacteria, e.g., formyl-methionylleucyl-phenylalanine (Allred & Hill 1978) and lipopolysaccharide (Forehand at al. 1991), of which the last also has been reported to be a potent inducer of IL-1b transcription (Cassatella et al 1997).…”

Section: Discussionmentioning

confidence: 99%

Expression of intracellular elastase activity in peripheral neutrophils from patients with adult periodontitis

Figueredo

Gustafsson

Åsman

et al. 2000

J Clinic Periodontology

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This study aimed to investigate whether circulating neutrophils from patients with periodontitis contain more catalytically active elastase than neutrophils from healthy controls. The amount of IL-1beta in these cells was also analyzed and the correlation with elastase activity was tested. The periodontitis group consisted of 15 subjects with marked periodontal destruction. The healthy control group consisted of 15 subjects with no clinical signs of periodontal destruction. The elastase activity and the IL-1beta content in the cells were measured with flow cytometry using a specific substrate and antibodies, respectively. The plasma concentration of IL-1beta and the total content of antigenic elastase in the crushed cells were measured with an ELISA. The elastase activity per neutrophil was significantly higher in the patients than in the controls, while the total antigenic elastase content did not differ. The % of cells positively stained for IL- 1beta was somewhat higher in the patient group. Significantly higher amounts of IL-1beta per sample, estimated by multiplying the % of stained cell with the amount of staining per cell, were found in the patient group. A significant correlation between IL-Ibeta and elastase activity was noted in the patient group (R=0.6, p=0.001), but not in the control group. In conclusion, peripheral neutrophils from patients with adult periodontitis express more active elastase and total amounts of IL-1. The similar amounts of antigenic elastase suggests that this higher activity is possibly due to some kind of priming/activation already in the circulation.

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“…We have also shown (46) that synergy among cationic polypeptides, calcium ionophore, chemotactic factors, and lectins led to the generation of enhanced amounts of superoxide, hydrogen peroxide, and chemiluminescence by human neutrophils and suggested that the excessive generation of oxidants, under similar conditions, might represent models of tissue damage. Other studies have shown that neutrophils and macrophages "primed" either by chemotactic peptides (47), LPS (48), lysophosphatides (49,50), or by LTA (5!) generated synergistic amounts of hydrogen peroxide.…”

Section: Introductionmentioning

confidence: 99%

Synergism among oxidants, proteinases, phospholipases, microbial hemolysins, cationic proteins, and cytokines

et al. 1992

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A striking similarity exists between the pathogenetic properties of group A streptococci and those of activated mammalian professional phagocytes (neutrophils, macrophages). Both types of cells are endowed by the ability to adhere to target cells; to elaborate oxidants, hydrolases, and membrane-active agents (hemolysins, phospholipases); and to freely invade tissues and destroy cells. From the evolutionary point of view, streptococci might justifiably be considered the forefathers of "modern" leukocytes. Our earlier findings that synergy between a streptococcal hemolysin (streptolysin S, SLS) and a streptococcal thiol-dependent proteinase and between cytotoxic antibodies+complement and streptokinase-activated plasmin readily killed tumor cells, led us to hypothesize that by analogy to the pathogenetic mechanisms of streptococci, the mechanisms of tissue destruction initiated by activated leukocytes in inflammatory sites, as well as in tissues undergoing episodes of ischemia and reperfusion, might also be the result of the synergistic effects among leukocyte-derived oxidants, phospholipases, proteinases, cytokines, and cationic proteins. The current report extends our previous synergy studies with endothelial cells to two additional cell types--monkey kidney epithelial cells and rat beating heart cells. Monolayers of 51Cr-labeled cells that had been treated by combinations of sublytic amounts of hydrogen peroxide (generated either by glucose oxidase, xanthine-xanthine oxidase, or by paraquat) and with sublytic amounts of a variety of membrane-active agents (streptolysin S, phospholipases A2 and C, lysophosphatides, histone, chlorhexidine) were killed in a synergistic manner (double synergy). Crystalline trypsin markedly enhanced cell killing by combinations of oxidant and the membrane-active agents (triple synergy). Injury to the cells was characterized by the appearance of large membrane blebs that detached from the cells and floated freely in the media, looking like lipid droplets. Cytotoxicity induced by the various combinations of agonists was depressed, to a large extent, by scavengers of hydrogen peroxide (catalase, dimethyl thiourea, and by Mn2+) but not by SOD or by deferoxamine. When cationic agents were employed together with hydrogen peroxide, polyanions (heparin, polyanethole sulfonate) were also found to inhibit cell killing. It is proposed that in order to effectively combat the deleterious toxic effects of leukocyte-derived agonists on cells and tissues, antagonistic "cocktails" comprised of cationized catalase, cationized SOD, dimethylthiourea, Mn(2+)+glycine, proteinase inhibitors, putative inhibitors of phospholipases, and polyanions might be concocted. The current literature on synergistic phenomena pertaining to mechanisms of cell and tissue injury in inflammation is selectively reviewed.

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Mechanisms of Lipopolysaccharide Priming for Enhanced Respiratory Burst Activity in Human Neutrophils

Cited by 11 publications

References 29 publications

A two-insult in vitro model of PMN-mediated pulmonary endothelial damage: requirements for adherence and chemokine release

A two-insult in vitro model of PMN-mediated pulmonary endothelial damage: requirements for adherence and chemokine release

Expression of intracellular elastase activity in peripheral neutrophils from patients with adult periodontitis

Synergism among oxidants, proteinases, phospholipases, microbial hemolysins, cationic proteins, and cytokines

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