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Circulating monocytes from healthy individuals and COPD patients
Ruta Aldonyte, Lennart Jansson, Eeva Piitulainen, Sabina Janciauskiene
Respiratory Research , 2003, DOI: 10.1186/1465-9921-4-11
Abstract: We investigated the basal and LPS-stimulated release of pro-inflammatory molecules from blood monocytes isolated from age and gender matched healthy (n = 30) and COPD (n = 20) individuals with and without AAT deficiency.After 18 h of cell culture the basal release of MMP-9 was 2.5-fold, p < 0.02 greater, whereas IL-8 was 1.8-fold (p < 0.01) lower from COPD patient monocytes than from controls. LPS-stimulated release of IL-6 and MCP-1 was greater from COPD patient's monocytes relative to controls, while activation of control cells resulted in enhanced secretion of ICAM-1 and MMP-9 compared to COPD patients. Independent of disease status, monocytes from PiZZ AAT carriers released less TNFα (by 2.3-fold, p < 0.03).The basal and LPS-stimulated secretion of specific pro-inflammatory molecules from circulating monocytes differs between healthy and COPD subjects. These findings may be valuable for further studies on the mechanisms involved in recruitment and activation of inflammatory cells in COPD.Chronic obstructive pulmonary disease (COPD) is a complex disease caused by various genetic and environmental risk factors acting singly or in concert. Severe alpha1-antitrypsin (AAT) deficiency, which results from a PiZZ genotype, is a well-known genetic risk factor associated with the development of early onset COPD [1]. Although it has been shown in a large number of AAT deficient individuals that smokers suffer more severe pulmonary impairment at an early age compared to non-smokers [2], the development of COPD in AAT deficient subjects, even among current or ex-smokers, is not universal [3]. Tobacco smoking represents the most important environmental risk factor for respiratory diseases and it is the first risk factor for COPD [4,5]. However, only about 20% of individuals who are smokers and have the normal PiMM genotype of AAT will develop COPD [3]. These findings lead to the idea that a combination of environmental factors, such as smoking, air pollution, childhood respir
Transcriptome Kinetics of Circulating Neutrophils during Human Experimental Endotoxemia  [PDF]
Stan de Kleijn, Matthijs Kox, Iziah Edwin Sama, Janesh Pillay, Angela van Diepen, Martijn A. Huijnen, Johannes G. van der Hoeven, Gerben Ferwerda, Peter W. M. Hermans, Peter Pickkers
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0038255
Abstract: Polymorphonuclear cells (neutrophils) play an important role in the systemic inflammatory response syndrome and the development of sepsis. These cells are essential for the defense against microorganisms, but may also cause tissue damage. Therefore, neutrophil numbers and activity are considered to be tightly regulated. Previous studies have investigated gene transcription during experimental endotoxemia in whole blood and peripheral blood mononuclear cells. However, the gene transcription response of the circulating pool of neutrophils to systemic inflammatory stimulation in vivo is currently unclear. We examined neutrophil gene transcription kinetics in healthy human subjects (n = 4) administered a single dose of endotoxin (LPS, 2 ng/kg iv). In addition, freshly isolated neutrophils were stimulated ex vivo with LPS, TNFα, G-CSF and GM-CSF to identify stimulus-specific gene transcription responses. Whole transcriptome microarray analysis of circulating neutrophils at 2, 4 and 6 hours after LPS infusion revealed activation of inflammatory networks which are involved in signaling of TNFα and IL-1α and IL-1β. The transcriptome profile of inflammatory activated neutrophils in vivo reflects extended survival and regulation of inflammatory responses. These changes in neutrophil transcriptome suggest a combination of early activation of circulating neutrophils by TNFα and G-CSF and a mobilization of young neutrophils from the bone marrow.
The Effects of Exercise on Judoists’ Circulating Blood Neutrophils
Zar A.,Karimi F.,Hovanloo F.,Ansian A.
Qom University of Medical Sciences Journal , 2010,
Abstract: Background and Objectives: Type, intensity and duration of exercises exert pivotal effects on athletes’ immune system and probably athletes’ susceptibility to upper respiratory tract infections. In this study we examined the effects of one session of moderate-intensity exercise on male judoists’ circulating blood neutrophil counts (BNC) and respiratory burst, and self-reported upper respiratory clinical infections 24 hours after the exercise and during the sport seasons.Methods: Ten male judoists after obtaining informed consent were included in the study. The athletes took part in a session of moderate-intensity exercise (60 minutes running on a treadmill) at 60% of maximum heart rate. Blood samples were drawn at rest immediately after the exercise. Blood neutrophil count and percentage of Phorbol Myristate Acetate (PMA) stimulated neutrophils in whole blood were assessed [as a marker of oxidative burst (OB) quality]. Athletes were asked about any signs of upper respiratory infections 24 hours after the exercise and during sport seasons. Paired-t test was used for statistical analysis and statistical significance was set at p<0.05.Results: BNC were in normal range at rest, and meaningfully increased immediately after the exercise (p<0.05). At rest, the OB activity was in normal range, and increased immediately after the exercise (not significant). During 24 hours after the exercise, athletes showed no signs of upper respiratory system infections. Also they mentioned no history of increased susceptibility of upper respiratory infections during sport seasons. Conclusion: Continuous judo exercises have no negative effects on BNC and OB activity. This finding is in accordance with the absence of self-reported upper respiratory infections in judoists during sport seasons. Significant increase in BNC after a session of exercise was a predictable event as a normal response of immune system to exercise stress. Normal OB activity after the exercise was in accordance with the absence of any signs of upper respiratory infections in athletes during 24 hours after the exercise.Keywords: Sports, Exercise; Immune System; Recovery, Active; Recovery, Passive; Neutrophils; Respiratory Burst; Athletes; Judoists; Exercise, Moderate-Intensity.
The Effects of Exercise on Judoists’ Circulating Blood Neutrophils  [cached]
A Zar
Qom University of Medical Sciences Journal , 2012,
Abstract: Background and Objectives: Type, intensity and duration of exercises exert pivotal effects on athletes’ immune system and probably athletes’ susceptibility to upper respiratory tract infections. In this study we examined the effects of one session of moderate-intensity exercise on male judoists’ circulating blood neutrophil counts (BNC) and respiratory burst, and self-reported upper respiratory clinical infections 24 hours after the exercise and during the sport seasons. Methods: Ten male judoists after obtaining informed consent were included in the study. The athletes took part in a session of moderate-intensity exercise (60 minutes running on a treadmill) at 60% of maximum heart rate. Blood samples were drawn at rest immediately after the exercise. Blood neutrophil count and percentage of Phorbol Myristate Acetate (PMA) stimulated neutrophils in whole blood were assessed [as a marker of oxidative burst (OB) quality]. Athletes were asked about any signs of upper respiratory infections 24 hours after the exercise and during sport seasons. Paired-t test was used for statistical analysis and statistical significance was set at p<0.05. Results: BNC were in normal range at rest, and meaningfully increased immediately after the exercise (p<0.05). At rest, the OB activity was in normal range, and increased immediately after the exercise (not significant). During 24 hours after the exercise, athletes showed no signs of upper respiratory system infections. Also they mentioned no history of increased susceptibility of upper respiratory infections during sport seasons. Conclusion: Continuous judo exercises have no negative effects on BNC and OB activity. This finding is in accordance with the absence of self-reported upper respiratory infections in judoists during sport seasons. Significant increase in BNC after a session of exercise was a predictable event as a normal response of immune system to exercise stress. Normal OB activity after the exercise was in accordance with the absence of any signs of upper respiratory infections in athletes during 24 hours after the exercise.
Sputum neutrophils as a biomarker in COPD: findings from the ECLIPSE study
Dave Singh, Lisa Edwards, Ruth Tal-Singer, Stephen Rennard
Respiratory Research , 2010, DOI: 10.1186/1465-9921-11-77
Abstract: Sputum samples were obtained from 488 COPD patients within the ECLIPSE cohort. 359 samples were obtained at baseline, and 297 after 1 year. 168 subjects provided samples at both visits. Serum interleukin-6 (IL-6), IL-8, surfactant protein D and C-reactive protein levels were measured by immunoassays. Low-dose CT scans evaluated emphysema.Sputum neutrophil % increased with GOLD stage. There was a weak association between % sputum neutrophils and FEV1 % predicted (univariate r2 = 0.025 and 0.094 at baseline and year 1 respectively, p < 0.05 after multivariate regression). Similar weak but significant associations were observed between neutrophil % and health status measured using the St Georges Respiratory Questionairre. There were no associations between neutrophils and exacerbation rates or emphysema. Associations between sputum neutrophils and systemic biomarkers were non-significant or similarly weak. The mean change over 1 year in neutrophil % was an increase of 3.5%.Sputum neutrophil measurements in COPD are associated weakly with FEV1 % predicted and health status. Sputum neutrophil measurements were dissociated from exacerbation rates, emphysema and systemic inflammation.Chronic obstructive pulmonary disease (COPD) is a progressive inflammatory airway disease, the most important cause of which is cigarette smoking. COPD is characterised by persistent and progressive airway inflammation [1]. The standard method for classifying disease severity is the measurement of forced expiratory volume in 1 second (FEV1) [2]. However, there is a need for biomarkers that are reflective of the inflammatory mechanisms involved in disease pathogenesis [3]. Such biomarkers may be useful for monitoring disease progression, evaluating the effects of therapeutic interventions or identifying disease sub-phenotypes with different clinical characteristics.A hallmark feature of COPD is the increased numbers of pulmonary neutrophils that can secrete a wide range of pro-inflammatory cyto
Oxidative Burst of Circulating Neutrophils Following Traumatic Brain Injury in Human  [PDF]
Yiliu Liao, Peng Liu, Fangyuan Guo, Zhi-Yuan Zhang, Zhiren Zhang
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0068963
Abstract: Besides secondary injury at the lesional site, Traumatic brain injury (TBI) can cause a systemic inflammatory response, which may cause damage to initially unaffected organs and potentially further exacerbate the original injury. Here we investigated plasma levels of important inflammatory mediators, oxidative activity of circulating leukocytes, particularly focusing on neutrophils, from TBI subjects and control subjects with general trauma from 6 hours to 2 weeks following injury, comparing with values from uninjured subjects. We observed increased plasma level of inflammatory cytokines/molecules TNF-α, IL-6 and CRP, dramatically increased circulating leukocyte counts and elevated expression of TNF-α and iNOS in circulating leukocytes from TBI patients, which suggests a systemic inflammatory response following TBI. Our data further showed increased free radical production in leukocyte homogenates and elevated expression of key oxidative enzymes iNOS, COX-2 and NADPH oxidase (gp91phox) in circulating leukocytes, indicating an intense induction of oxidative burst following TBI, which is significantly greater than that in control subjects with general trauma. Furthermore, flow cytometry assay proved neutrophils as the largest population in circulation after TBI and showed significantly up-regulated oxidative activity and suppressed phagocytosis rate for circulating neutrophils following brain trauma. It suggests that the highly activated neutrophils might play an important role in the secondary damage, even outside the injured brain. Taken together, the potent systemic inflammatory response induced by TBI, especially the intensively increase oxidative activity of circulating leukocytes, mainly neutrophils, may lead to a systemic damage, dysfunction/damage of bystander tissues/organs and even further exacerbate secondary local damage. Controlling these pathophysiological processes may be a promising therapeutic strategy and will protect unaffected organs and the injured brain from the secondary damage.
A unique protein profile of peripheral neutrophils from COPD patients does not reflect cytokine-induced protein profiles of neutrophils in vitro
Jeroen D Langereis, René C Schweizer, Jan-Willem J Lammers, Leo Koenderman, Laurien H Ulfman
BMC Pulmonary Medicine , 2011, DOI: 10.1186/1471-2466-11-44
Abstract: Using fluorescence 2-dimensional difference gel electrophoresis we investigated differentially regulated proteins in peripheral neutrophils from COPD patients and healthy age-matched control subjects. Furthermore, protein profiles from COPD patients were compared with those of neutrophils of healthy age-matched controls that were stimulated with TNFα and/or GM-CSF in vitro. Protein gels were compared using DeCyder 7.0 software.We identified 7 significantly regulated protein spots between peripheral neutrophils from COPD patients and age-matched healthy control subjects. Stimulation of peripheral neutrophils with TNFα, GM-CSF or TNFα + GM-CSF in vitro resulted in 13, 20 and 22 regulated protein spots, respectively. However, these cytokine-induced protein differences did not correspond with the protein differences found in neutrophils from COPD patients.These results show that neutrophils from COPD patients have a unique protein profile compared to neutrophils from healthy age-matched controls. Furthermore, the neutrophil profiles of COPD patients do not reflect putative dominant signals induced by TNFα, GM-CSF or their combination. Our results indicate that systemic neutrophil responses in COPD patients are caused by a unique but subtle interplay between multiple inflammatory signals.COPD is classified by the guidelines of the Global Initiative for Chronic Obstructive Lung Disease, which is based on lung function parameters: forced expiratory volume in 1 second (FEV1) and forced vital capacity (FVC) [1]. However, it has become increasingly clear that the GOLD classification does not represent the complex local and systemic inflammation in COPD [2-4]. Part of this inflammatory process is the secretion of inflammatory mediators by lung epithelium, alveolar macrophages and other inflammatory cells [5]. These inflammatory mediators affect the local tissue and attract inflammatory cells to the site of inflammation. For instance, alveolar macrophages secrete tumor necrosis
Dysregulated apoptosis and NFκB expression in COPD subjects
Vanessa Brown, J Stuart Elborn, Judy Bradley, Madeleine Ennis
Respiratory Research , 2009, DOI: 10.1186/1465-9921-10-24
Abstract: Analysis of apoptosis in induced sputum was carried out by 3 methods; light microscopy, Annexin V/Propidium iodide and the terminal transferase-mediated dUTP nick end-labeling (TUNEL) method. Activation of NFκB was assessed using a flow cytometric method and the phosphorylation state of IκBα was carried out using the Bio-Rad Bio-Plex phosphoprotein IκBα assay.Flow cytometric analysis showed a significant reduction in the percentage of sputum neutrophils undergoing spontaneous apoptosis in healthy smokers and subjects with COPD compared to non-smokers (p < 0.001). Similar findings were demonstrated using the Tunel assay and in the morphological identification of apoptotic neutrophils. A significant increase was observed in the expression of both the p50 (p = 0.006) and p65 (p = 0.006) subunits of NFκB in neutrophils from COPD subjects compared to non-smokers.These results demonstrate that apoptosis is reduced in the sputum of COPD subjects and in healthy control smokers and may be regulated by an associated activation of NFκB.Chronic obstructive pulmonary disease (COPD) is characterised by an inflammatory infiltrate consisting mainly of neutrophils [1], with increased neutrophils and inflammatory mediators in both bronchial tissue and airways of COPD patients [2-4]. In several acute and chronic neutrophilic diseases, such as cystic fibrosis and acute respiratory distress syndrome (ARDS) there is a delay in neutrophil apoptosis resulting in persistent inflammation [5,6]. Studies investigating neutrophil apoptosis in COPD have mainly focussed on circulating neutrophils and shown a reduction in spontaneous apoptosis during an exacerbation of COPD that increases with treatment [7] or no changes in the rate of apoptosis of cultured blood neutrophils between stable COPD subjects, healthy smokers and healthy control non-smokers [8]. The only study to date investigating spontaneous neutrophil apoptosis in sputum from COPD subjects was unable to identify any differences in ap
Gender differences in predictors of health status in patients with COPD
Ferrari, Renata;Tanni, Suzana Erico;Lucheta, Paulo Adolfo;Faganello, Márcia Maria;Amaral, Renata Antonialli Ferreira do;Godoy, Irma;
Jornal Brasileiro de Pneumologia , 2010, DOI: 10.1590/S1806-37132010000100008
Abstract: objective: to evaluate the health status (hs) of copd patients and to identify the main predictors of hs in these patients according to gender. methods: the study included 90 copd patients (60 males and 30 females; mean age = 64 ± 9 years) with a wide range of airway obstruction disorders (mean fev1 = 56 ± 19% of predicted). the men were individually matched to the women by % of predicted fev1 (ratio: 2:1). the patients were assessed regarding body composition; six-minute walk distance; perception of dyspnea using the modified medical research council dyspnea scale; saint george's respiratory questionnaire (sgrq); charlson comorbidity index; and the multidimensional body mass index, airway obstruction, dyspnea, and exercise capacity (bode) index. multiple linear regression analysis was performed to identify the predictors of hs by gender. results: impairment of hs was greater among the women than among the men for sgrq total score and for all sgrq domains (total: 51 ± 18% vs. 38 ± 19%; p = 0.002; symptoms: 61 ± 22% vs. 42 ± 21%; p < 0.001; activity: 62 ± 18% vs. 49 ± 21%; p = 0.004; and impact: 41 ± 19% vs. 27 ± 18%; p = 0.001). the multiple linear regression showed that age and perception of dyspnea correlated with sgrq total score for both genders (males, r2 = 0.42; females, r2 = 0.70; p < 0.05). conclusions: our results showed an association between gender and hs in copd patients. age and dyspnea are determinants of hs in both genders.
Gender Differences in Plasma Biomarker Levels in a Cohort of COPD Patients: A Pilot Study  [PDF]
Juan P. de Torres,Ciro Casanova,Victor Pinto-Plata,Nerea Varo,Patricia Restituto,Elizabeth Cordoba-Lanus,Rebeca Baz-Dávila,Armando Aguirre-Jaime,Bartolome R. Celli
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0016021
Abstract: Little is known about gender differences in plasma biomarker levels in patients with chronic obstructive pulmonary disease (COPD).
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