Evaluation of IL-8 Nasal Lavage Levels and the Effects of Nasal Involvement on Disease Severity in Patients with Stable Chronic Obstructive Pulmonary Disease

Çelik, Hacer; Akpinar, Serdar; Karabulut, Hayriye; Oktar, Pinar; Dursun, Berna; Erguden, Huyla Celenk; Günay, Si̇bel; Şipit, Tuğrul

doi:10.1007/s10753-014-9968-0

Cited by 11 publications

(9 citation statements)

References 26 publications

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“…In the 50 FORTE study participants discussed above, IL-2 was higher in COPD patients, but was lower in rapid decliners compared to stable COPD patients [ 44 ]. Similarly, in small studies IL-8 has been reported to be elevated in COPD patients in smaller studies with less than 100 subjects [ 57 , 58 ]. This is the first large study to show that IL-8 is independently associated with progression of emphysema by CT scan and additional studies in independent longitudinal COPD cohorts should consider measuring IL-8.…”

Section: Discussionmentioning

confidence: 98%

The value of blood cytokines and chemokines in assessing COPD

et al. 2017

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BackgroundBlood biomarkers are increasingly used to stratify high risk chronic obstructive pulmonary disease (COPD) patients; however, there are fewer studies that have investigated multiple biomarkers and replicated in multiple large well-characterized cohorts of susceptible current and former smokers.MethodsWe used two MSD multiplex panels to measure 9 cytokines and chemokines in 2123 subjects from COPDGene and 1117 subjects from SPIROMICS. These biomarkers included: interleukin (IL)-2, IL-6, IL-8, IL-10, tumor necrosis factor (TNF)-α, interferon (IFN)-γ, eotaxin/CCL-11, eotaxin-3/CCL-26, and thymus and activation-regulated chemokine (TARC)/CCL-17. Regression models adjusted for clinical covariates were used to determine which biomarkers were associated with the following COPD phenotypes: airflow obstruction (forced expiratory flow at 1 s (FEV1%) and FEV1/forced vital capacity (FEV1/FVC), chronic bronchitis, COPD exacerbations, and emphysema. Biomarker-genotype associations were assessed by genome-wide association of single nucleotide polymorphisms (SNPs).ResultsEotaxin and IL-6 were strongly associated with airflow obstruction and accounted for 3–5% of the measurement variance on top of clinical variables. IL-6 was associated with progressive airflow obstruction over 5 years and both IL-6 and IL-8 were associated with progressive emphysema over 5 years. None of the biomarkers were consistently associated with chronic bronchitis or COPD exacerbations. We identified one novel SNP (rs9302690 SNP) that was associated with CCL17 plasma measurements.ConclusionWhen assessing smoking related pulmonary disease, biomarkers of inflammation such as IL-2, IL-6, IL-8, and eotaxin may add additional modest predictive value on top of clinical variables alone.Trial registrationCOPDGene (ClinicalTrials.gov Identifier: NCT02445183).Subpopulations and Intermediate Outcomes Measures in COPD Study (SPIROMICS) (ClinicalTrials.gov Identifier: NCT 01969344).Electronic supplementary materialThe online version of this article (10.1186/s12931-017-0662-2) contains supplementary material, which is available to authorized users.

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Section: Discussionmentioning

confidence: 98%

The value of blood cytokines and chemokines in assessing COPD

et al. 2017

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“…IL-8 is a major chemoattractant to neutrophils, which are responsible for inducing and sustaining the inflammatory state [ 16 ]. A close correlation between the number of neutrophils in induced sputum in COPD patients, the IL-8 level, and clinical outcome of the illness has been reported [ 17 ]. On the contrary, neutralization of IL-8 by a monoclonal antibody recognizing IL-8 in COPD causes a decrease of exacerbation frequency and clinical symptoms [ 18 ].…”

Section: Introductionmentioning

confidence: 92%

Chemical constituents of tobacco smoke induce the production of interleukin-8 in human bronchial epithelium, 16HBE cells

Zhou¹,

Xiao²,

Xu³

et al. 2016

Tob. Induced Dis.

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BackgroundInterleukin-8 (IL-8) functions as a major chemoattractant and plays pivotal roles in the initiation and development of chronic obstructive pulmonary disease (COPD), and tobacco smoke is a most risk factor contributing to the development of COPD. Hence, we have screened some of the tobacco smoke-derived chemical compounds that potentially induce the production of IL-8 in human bronchial epithelium, 16HBE cells.MethodsTwenty-eight hazardous smoke components belonging to 9 classes including nicotine, ammonia, aromatic amines, polycyclic aromatic hydrocarbons, phenols, carbonyls, hydrocyanic acid, nitrosamines and other volatile organics were used in the experiments. Proliferation of 16HBE cells was determined by cell counting kit-8 kit, luciferase activity was measured in IL-8 reporter gene-expressing 16HBE cells, and IL-8 levels in culture supernatants were quantified by enzyme-linked immunosorbent assay.ResultsAt the non-toxic dosages, chemical compounds belonging to nicotine, aromatic amines, benzopyrene, phenols, aldehydes, and some other volatile organics dose-dependently increased IL-8 reporter gene expression. Consistently, the representative compounds belonging to nicotine, aromatic amines, benzopyrene, phenols, aldehydes, and some other volatile organics significantly and dose-dependently increased IL-8 levels in the culture supernatants of 16HBE cells, among these compounds, benzopyrene is a most potent stimulator for inducing IL-8 production.ConclusionsThe present study has identified particular tobacco smoke constituents responsible for inducing the IL-8 production in human bronchial epithelium, which might help shed light on the pathogenesis of tobacco smoke-induced COPD.

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“…Both IL-1β and IL-6 mediate inflammation by binding to their respective receptors on endothelial cells to induce the expression of leukocyte adhesion molecules such as ICAM-1. ICAM-1 interacts with counter receptors on the surface of leukocytes to mediate the migration of leukocytes, and it is also involved in the arrest of leukocytes on inflamed endothelium (Lesniak et al 2013 ; Winter et al 2002 ; Celic et al 2015 ). The macrophage inhibitory protein 1a (MIP1a) takes part in the leukocyte chemotaxis and correlates with IL-8 (Gamucci et al 2014 ).…”

Section: Discussionmentioning

confidence: 99%

The effect of different workplace nanoparticles on the immune systems of employees

et al. 2017

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Currently, nanoparticles are widely present in the environment and are being used in various industrial technologies. Nanoparticles affect immune functions, causing different immune responses. The aim of the current study was to evaluate several cytokines, interleukin (IL)-1b, IL-6, IL-8, tumour necrosis factor-a (TNF-α), interferon-γ, adhesive molecule sICAM-1, macrophage inhibitory protein 1a (MIP1a) and secretory immunoglobulin A, in nasal lavage fluid and in the peripheral blood of healthy subjects exposed to workplace nanoparticles. Thirty-six employees from three different environments were examined: 12 from a metalworking company, 12 from a woodworking company and 12 office workers. The nanoparticles in the different workplaces were detected in the air in the immediate vicinity of the employees. The particle number concentration and surface area values were significantly higher in the workplaces of the metal- and woodworking industries, but concentrations of mass were lower (the measurements were performed by an electrical low-pressure impactor ELPI+). Energy dispersive X-ray spectroscopy (EDS, an attachment to a high-resolution SEM) was used to provide elemental analysis or chemical characterization of the dust particles in a low-vacuum field-free mode operating at a potential of 15 kV spot 3.0. The technique used provided quantitative and spatial analyses of the distribution of elements through mapping (two to three parallel measurements) and point analysis (four to five parallel measurements). Samples from the metal industry contained more ultramicroscopic and nanometric particles, e.g. toxic metals such as Zn, Mn and Cr, and fewer microscopic dust particles. The nasal lavage and peripheral blood were taken at the beginning and the end of the working week, when immune indices were measured. Our data showed a statistically significant increased level of the pro-inflammatory cytokine TNF-α in serum in both exposed groups compared with office workers as well as a higher level of TNF-α in workers from the woodworking company compared with the metalworking employees. We found an elevated level of IL-6 in the exposed groups as well as an elevated level of IL-8 in the nasal lavage in woodworking employees after work.

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Evaluation of IL-8 Nasal Lavage Levels and the Effects of Nasal Involvement on Disease Severity in Patients with Stable Chronic Obstructive Pulmonary Disease

Cited by 11 publications

References 26 publications

The value of blood cytokines and chemokines in assessing COPD

The value of blood cytokines and chemokines in assessing COPD

Chemical constituents of tobacco smoke induce the production of interleukin-8 in human bronchial epithelium, 16HBE cells

The effect of different workplace nanoparticles on the immune systems of employees

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