Other search tools

About this data

The publication data currently available has been vetted by Vanderbilt faculty, staff, administrators and trainees. The data itself is retrieved directly from NCBI's PubMed and is automatically updated on a weekly basis to ensure accuracy and completeness.

If you have any questions or comments, please contact us.

Results: 1 to 6 of 6

Publication Record

Connections

Neutrophil-generated oxidative stress and protein damage in Staphylococcus aureus.
Beavers WN, Skaar EP
(2016) Pathog Dis 74:
MeSH Terms: Animals, Gene Expression Regulation, Host-Pathogen Interactions, Humans, Microbial Viability, Neutrophils, Nitric Oxide, Oxidants, Oxidation-Reduction, Oxidative Stress, Respiratory Burst, Staphylococcal Infections, Staphylococcus aureus
Show Abstract · Added April 8, 2017
Staphylococcus aureus is a ubiquitous, versatile and dangerous pathogen. It colonizes over 30% of the human population, and is one of the leading causes of death by an infectious agent. During S. aureus colonization and invasion, leukocytes are recruited to the site of infection. To combat S. aureus, leukocytes generate an arsenal of reactive species including superoxide, hydrogen peroxide, nitric oxide and hypohalous acids that modify and inactivate cellular macromolecules, resulting in growth defects or death. When S. aureus colonization cannot be cleared by the immune system, antibiotic treatment is necessary and can be effective. Yet, this organism quickly gains resistance to each new antibiotic it encounters. Therefore, it is in the interest of human health to acquire a deeper understanding of how S. aureus evades killing by the immune system. Advances in this field will have implications for the design of future S. aureus treatments that complement and assist the host immune response. In that regard, this review focuses on how S. aureus avoids host-generated oxidative stress, and discusses the mechanisms used by S. aureus to survive oxidative damage including antioxidants, direct repair of damaged proteins, sensing oxidant stress and transcriptional changes. This review will elucidate areas for studies to identify and validate future antimicrobial targets.
© FEMS 2016. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.
0 Communities
1 Members
0 Resources
13 MeSH Terms
A printed superoxide dismutase coated electrode for the study of macrophage oxidative burst.
Hiatt LA, McKenzie JR, Deravi LF, Harry RS, Wright DW, Cliffel DE
(2012) Biosens Bioelectron 33: 128-33
MeSH Terms: Animals, Biosensing Techniques, Calibration, Cells, Cultured, Electrochemical Techniques, Electrodes, Macrophages, Mice, Microfluidic Analytical Techniques, Reproducibility of Results, Respiratory Burst, Superoxide Dismutase, Tetradecanoylphorbol Acetate
Show Abstract · Added January 20, 2015
The miniaturization of electrochemical sensors allows for the minimally invasive and cost effective examination of cellular responses at a high efficacy rate. In this work, an ink-jet printed superoxide dismutase electrode was designed, characterized, and utilized as a novel microfluidic device to examine the metabolic response of a 2D layer of macrophage cells. Since superoxide production is one of the first indicators of oxidative burst, macrophage cells were exposed within the microfluidic device to phorbol myristate acetate (PMA), a known promoter of oxidative burst, and the production of superoxide was measured. A 46 ± 19% increase in current was measured over a 30 min time period demonstrating successful detection of sustained macrophage oxidative burst, which corresponds to an increase in the superoxide production rate by 9 ± 3 attomoles/cell/s. Linear sweep voltammetry was utilized to show the selectivity of this sensor for superoxide over hydrogen peroxide. This novel controllable microfluidic system can be used to study the impact of multiple effectors from a large number of bacteria or other invaders along a 2D layer of macrophages, providing an in vitro platform for improved electrochemical studies of metabolic responses.
Copyright © 2011 Elsevier B.V. All rights reserved.
0 Communities
1 Members
0 Resources
13 MeSH Terms
Endotoxin priming of neutrophils requires NADPH oxidase-generated oxidants and is regulated by the anion transporter ClC-3.
Moreland JG, Davis AP, Matsuda JJ, Hook JS, Bailey G, Nauseef WM, Lamb FS
(2007) J Biol Chem 282: 33958-67
MeSH Terms: Anaerobiosis, Animals, Cell Line, Chloride Channels, Enzyme Activation, Humans, Lipopolysaccharides, Mice, N-Formylmethionine Leucyl-Phenylalanine, NADPH Oxidases, Neisseria meningitidis, Neutrophil Activation, Neutrophils, Oxidation-Reduction, Respiratory Burst, Secretory Vesicles, p38 Mitogen-Activated Protein Kinases
Show Abstract · Added February 22, 2016
Several soluble mediators, including endotoxin, prime neutrophils for an enhanced respiratory burst in response to subsequent stimulation. Priming of neutrophils occurs in vitro, and primed neutrophils are found in vivo. We previously localized the anion transporter ClC-3 to polymorphonuclear leukocytes (PMN) secretory vesicles and demonstrated that it is required for normal NADPH oxidase activation in response to both particulate and soluble stimuli. We now explore the contribution of the NADPH oxidase and ClC-3 to endotoxin-mediated priming. Lipooligosaccharide (LOS) from Neisseria meningitidis enhances the respiratory burst in response to formyl-Met-Leu-Phe, an effect that was impaired in PMNs lacking functional ClC-3 and under anaerobic conditions. Mobilization of receptors to the cell surface and phosphorylation of p38 MAPK by LOS were both impaired in PMN with the NADPH oxidase chemically inhibited or genetically absent and in cells lacking functional ClC-3. Furthermore, inhibition of the NADPH oxidase or ClC-3 in otherwise unstimulated cells elicited a phenotype similar to that seen after endotoxin priming, suggesting that basal oxidant production helps to maintain cellular quiescence. In summary, NADPH oxidase activation was required for LOS-mediated priming, but basal oxidants kept unstimulated cells from becoming primed. ClC-3 contributes to both of these processes.
0 Communities
1 Members
0 Resources
17 MeSH Terms
C242T CYBA polymorphism of the NADPH oxidase is associated with reduced respiratory burst in human neutrophils.
Wyche KE, Wang SS, Griendling KK, Dikalov SI, Austin H, Rao S, Fink B, Harrison DG, Zafari AM
(2004) Hypertension 43: 1246-51
MeSH Terms: Adult, Alleles, Amino Acid Substitution, Arteriosclerosis, Codon, Female, Genetic Predisposition to Disease, Genotype, Humans, Male, Membrane Transport Proteins, Middle Aged, NADPH Dehydrogenase, NADPH Oxidases, Neutrophils, Oxidative Stress, Phosphoproteins, Polymorphism, Single Nucleotide, Respiratory Burst, Superoxides, Tetradecanoylphorbol Acetate
Show Abstract · Added March 26, 2019
Oxidative stress contributes to the pathogenesis of atherosclerosis. p22phox-based NAD(P)H oxidases exist in the vessel wall, acting as important superoxide-generating systems in the vasculature. Some studies have identified reduced atherosclerosis in the presence of the C242T CYBA polymorphism, whereas others have not. Because vascular p22phox is identical to neutrophil p22phox, we studied the association between the C242T, A640G, and -930A/G CYBA polymorphisms and the quantity of superoxide produced from neutrophils isolated from healthy adults to determine if these polymorphisms had any functional impact on NADPH oxidase function. Neutrophils were isolated from 90 subjects by Percoll density gradient centrifugation. Genotypes were determined by polymerase chain reaction (PCR) and restriction mapping, as well as real-time PCR. The oxidative burst was stimulated with phorbol 12-myristate 13-acetate. Superoxide was quantified using the superoxide dismutase inhibitable oxidation of the spin probe hydroxylamine 1-hydroxy-3-carboxy-pyrrolidine, detected by electron paramagnetic resonance. Superoxide production was significantly affected by the C242T polymorphism, being 8.7+/-0.7, 7.9+/-0.6, and 5.9+/-1.2 micromol/L per minute per 10(6) neutrophils for the C242T CC, CT, and TT genotypes, respectively (P<0.05). In contrast, the A640G and the -930A/G polymorphisms did not alter the neutrophil respiratory burst. Phagocytic respiratory burst activity in homozygous individuals with the T allele of the C242T CYBA polymorphism is significantly lower than of wild-type carriers and heterozygous individuals. Because p22phox exists in both the neutrophil and vessel wall, vascular oxidative stress is likely diminished in individuals with this polymorphism.
0 Communities
1 Members
0 Resources
MeSH Terms
Absence of angiotensin II type 1 receptor in bone marrow-derived cells is detrimental in the evolution of renal fibrosis.
Nishida M, Fujinaka H, Matsusaka T, Price J, Kon V, Fogo AB, Davidson JM, Linton MF, Fazio S, Homma T, Yoshida H, Ichikawa I
(2002) J Clin Invest 110: 1859-68
MeSH Terms: Animals, Bone Marrow Transplantation, Cell Movement, Collagen Type I, Collagen Type III, Extracellular Matrix, Fibrosis, Hematopoietic Stem Cells, Kidney, Kidney Diseases, Macrophages, Male, Matrix Metalloproteinase 2, Mice, Mice, Inbred C57BL, Mice, Knockout, Phagocytosis, Receptor, Angiotensin, Type 1, Receptors, Angiotensin, Respiratory Burst, Tissue Inhibitor of Metalloproteinase-1, Transforming Growth Factor beta, Transforming Growth Factor beta1, Ureteral Obstruction
Show Abstract · Added December 10, 2013
We examined the in vivo function of the angiotensin II type 1 receptor (Agtr1) on macrophages in renal fibrosis. Fourteen days after the induction of unilateral ureteral obstruction (UUO), wild-type mice reconstituted with marrow lacking the Agtr1 gene (Agtr1(-/-)) developed more severe interstitial fibrosis with fewer interstitial macrophages than those in mice reconstituted with Agtr1(+/+) marrow. These differences were not observed at day 5 of UUO. The expression of profibrotic genes - including TGF-beta1, alpha1(I) collagen, and alpha1(III) collagen - was substantially higher in the obstructed kidneys of mice with Agtr1(-/-) marrow than in those with Agtr1(+/+) marrow at day 14 but not at day 5 of UUO. Mice with Agtr1(-/-) marrow were characterized by reduced numbers of peripheral-blood monocytes and macrophage progenitors in bone marrow. In vivo assays revealed a significantly impaired phagocytic capability in Agtr1(-/-) macrophages. In vivo treatment of Agtr1(+/+) mice with losartan reduced phagocytic capability of Agtr1(+/+) macrophages to a level comparable to that of Agtr1(-/-) macrophages. Thus, during urinary tract obstruction, the Agtr1 on bone marrow-derived macrophages functions to preserve the renal parenchymal architecture, and this function depends in part on its modulatory effect on phagocytosis.
1 Communities
5 Members
0 Resources
24 MeSH Terms
Intradialytic granulocyte reactive oxygen species production: a prospective, crossover trial.
Himmelfarb J, Ault KA, Holbrook D, Leeber DA, Hakim RM
(1993) J Am Soc Nephrol 4: 178-86
MeSH Terms: Adult, Aged, Aged, 80 and over, Cellulose, Complement Activation, Disease Susceptibility, Endothelium, Vascular, Female, Flow Cytometry, Granulocytes, Humans, Infection, Male, Membranes, Artificial, Methylmethacrylates, Middle Aged, Prospective Studies, Reactive Oxygen Species, Renal Dialysis, Respiratory Burst, Staphylococcus aureus, Tetradecanoylphorbol Acetate
Show Abstract · Added May 20, 2014
By the use of flow cytometric techniques, this prospective, randomized crossover study was designed to analyze intradialytic granulocyte reactive oxygen species (ROS) formation in whole blood with complement-activating and noncomplement-activating hollow fiber membranes. Dialysis with a complement-activating membrane resulted in a 6.5-fold increase in granulocyte hydrogen peroxide production 15 min after dialysis initiation and remained significantly elevated (P < 0.01) through the first 30 min with this membrane in comparison to both predialysis values and simultaneous values with a noncomplement-activating membrane. Further studies demonstrated that blood obtained at 15 min with a complement-activating membrane generated significantly less granulocyte ROS production in response to Staphylococcus aureus incubation than blood obtained either predialysis or at the same time in dialysis with a noncomplement-activating membrane. Both complement-activating and noncomplement-activating dialysis membranes caused slightly decreased granulocyte responsiveness to phorbol myristate acetate. It was concluded that hemodialysis with complement-activating membranes results in increased granulocyte ROS production and decreased responsiveness to S. aureus challenge during the dialysis procedure. These results document the potential role of ROS in hemodialysis-associated pathology and susceptibility to infection.
0 Communities
1 Members
0 Resources
22 MeSH Terms