Flow–Cytometric Evaluation of Oxidative Burst in Phagocytic Cells of Children with Cystic Fibrosis

Frühwirth, Martin; Ruedl, Christiane; Ellemunter, Helmut; Böck, Günther; Wolf, H.

doi:10.1159/000024022

Cited by 24 publications

(20 citation statements)

References 13 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In fact, Gln supplementation in vitro enhances both phagocytosis and ROS production in isolated neutrophils (34) and, in vivo, suppresses IL-8 production by neutrophils (35). Inasmuch as an increased IL-8 production (33) and oxidative burst alterations (36) have been reported in circulating neutrophils from CF patients, the Gln intracellular depletion found in our study may explain these alterations. However, the exact role of neutrophil Gln depletion in the pathogenesis of CF remains to be elucidated.…”

Section: Discussionsupporting

confidence: 61%

Neutrophil Glutamine Deficiency in Relation to Genotype in Children with Cystic Fibrosis

et al. 2006

View full text Add to dashboard Cite

Pulmonary disease in cystic fibrosis (CF) is characterized by a chronic neutrophil-dominated inflammation of lung tissue. Inasmuch as some amino acids (AA) play a pivotal role in various aspects of neutrophil metabolism, the aim of this study was to investigate a possible alteration of neutrophil AA metabolism and to evaluate its relation (if any) with the genotype. We performed plasma and neutrophil AA analysis in 26 CF patients with known genotype, 10 patients with non-CF bronchiectasis, and 20 normal subjects. The CF group showed a significant decrease of free intracellular neutrophil glutamine (Gln) content compared with controls and the non-CF bronchiectasis group. In the latter group, levels of neutrophil Gln were significantly lower compared with the controls. Amino acid plasma concentration in non-CF bronchiectasis showed a decrease of Gln and taurine compared with controls. Neutrophil Gln content showed values significantly lower in CF patients with severe mutations (class I, II, and III mutations) compared with mild mutations (class IV and V mutations). Results of our study add further evidence for intrinsic neutrophil alterations that could play an important role in the pathogenesis of chronic pulmonary disease in CF patients. (Pediatr Res 59: 13-16, 2006)

show abstract

Section: Discussionsupporting

confidence: 61%

Neutrophil Glutamine Deficiency in Relation to Genotype in Children with Cystic Fibrosis

et al. 2006

View full text Add to dashboard Cite

show abstract

“…Earlier work has demonstrated a decreased release of reactive oxygen species from CF neutrophils in response to fMLP compared to controls [27]. Studies using PMA and zymosan found that, in some CF patients, oxidative activity was higher than in controls, but in other patients, it was found to be lower than controls, indicating that there was extensive heterogeneity in oxidative activity [29].…”

Section: Discussionmentioning

confidence: 96%

Effect of cystic fibrosis exacerbations on neutrophil function

Brockbank

Downey

Elborn

et al. 2005

International Immunopharmacology

View full text Add to dashboard Cite

In cystic fibrosis (CF), inflammation is caused by persistent bacterial infection from Pseudomonas aeruginosa and Burkholderia cenocepacia in the lung and is characterised by the persistent infiltration of massive numbers of neutrophils which leads to lung injury. The aim of this present study was to investigate the effects of CF exacerbations on the reactivity of peripheral blood neutrophils compared to data from a normal healthy control population. Peripheral blood neutrophils were isolated from control subjects and CF patients before and after an exacerbation of their lung disease. Isolated neutrophils were stimulated with N-formyl-methionyl-leucyl-phenylalanine (fMLP) and phorbol 12-myristate 13-acetate (PMA) and the rate of superoxide generation and elastase activity measured and compared with neutrophils from healthy age-matched controls. Neutrophils from CF patients spontaneously generated higher levels of superoxide after resolution of the exacerbation compared to control neutrophils. The stimulated generation of superoxide from control neutrophils was not significantly different from neutrophils isolated from CF patients either before or after resolution of the CF exacerbation. Neutrophils from CF patients spontaneously released more elastase than control neutrophils but released less elastase than control neutrophils in response to fMLP. The stimulated release of elastase from neutrophils was not significantly different before compared to after resolution of the exacerbation. Neutrophils from CF patients displayed a different pattern of response than those from control subjects; however, CF exacerbations did not appear to modulate neutrophil function. D

show abstract

“…Whether failure to kill pathogens results from a primary abnormality of CF neutrophil function, a secondary neutrophil defect related to the CF pulmonary microenvironment, a neutrophil-independent factor, or from a combinatorial effect, is at present unclear. The neutrophil respiratory burst, which results in the generation of potentially injurious oxygen radicals, has been reported to be elevated in cells isolated from CF patients [10]; in other studies the response has been shown to vary according to the infecting pathogen [31] or to the method employed to detect respiratory burst activity [11], and secretory products of Pseudomonas aeruginosa have been reported to suppress neutrophil respiratory burst activity [32]. In this study, we have employed three methods (cytochrome C reduction, lum-DCL and luc-DCL) to quantify the respiratory burst activity of neutrophils isolated (by a method demonstrated to cause minimal disturbance of neutrophil function [24]) from a macrolide-naïve homogeneous patient group (DF508 homozygotes colonised with Pseudomonas aeruginosa) and have demonstrated unequivocally that, in response to soluble ligand stimulation, oxidant output is identical to that from neutrophils from healthy volunteers.…”

Section: Discussionmentioning

confidence: 98%

Cystic fibrosis neutrophils have normal intrinsic reactive oxygen species generation

McKeon¹,

Cadwallader²,

Idris³

et al. 2009

European Respiratory Journal

View full text Add to dashboard Cite

Previous studies have identified abnormalities in the oxidative responses of the neutrophil in cystic fibrosis (CF), but it is unclear whether such changes relate to loss of membrane cystic fibrosis transmembrane conductance regulator (CFTR) or to the inflammatory environment present in this disease. The aim of the present study was to determine whether neutrophils from CF patients demonstrate an intrinsic abnormality of the respiratory burst.The respiratory burst activity of neutrophils isolated from stable DF508 homozygote CF patients and matched healthy controls was quantified by both chemiluminscence and cytochrome C reduction. Expression of NADPH oxidase components and CFTR was determined by Western blotting and RT-PCR.The oxidative output from neutrophils from CF in response to receptor-linked and particulate stimuli did not differ from that of controls. Expression of NADPH oxidase components was identical in CF and non-CF neutrophils. While low levels of CFTR mRNA could be identified in the normal human neutrophil, we were unable to detect CFTR protein in human neutrophil lysates or immunoprecipitates.CFTR has no role in controlling neutrophil oxidative activity; previously reported differences in neutrophil function between CF and non-CF subjects most likely relate to the inflammatory milieu from which the cells were isolated.

show abstract

Flow–Cytometric Evaluation of Oxidative Burst in Phagocytic Cells of Children with Cystic Fibrosis

Cited by 24 publications

References 13 publications

Neutrophil Glutamine Deficiency in Relation to Genotype in Children with Cystic Fibrosis

Neutrophil Glutamine Deficiency in Relation to Genotype in Children with Cystic Fibrosis

Effect of cystic fibrosis exacerbations on neutrophil function

Cystic fibrosis neutrophils have normal intrinsic reactive oxygen species generation

Contact Info

Product

Resources

About