interleukin-8 and Respiration-Disorders

Exposure to high concentrations of copper is associated with pulmonary inflammation and chronic respiratory disease (CRD). Epigenetic modulation of noncoding RNAs contributes to the development of several CRDs. It is unknown whether epigenetic modulation is involved in copper mediated pulmonary inflammation and CRD. We conducted a case-control study of 101 CRD cases and 161 control subjects in Shijiazhuang, China, and evaluated circRNAs and cytokine levels (IL-6 and IL-8) by qPCR and ELISA. Urinary copper concentration was determined by inductively coupled plasma mass spectrometry. Linear mixed models and generalized linear mixed models were used to assess the associations of circRNAs with CRD, urinary copper, and cytokines. We exposed the human bronchial epithelial cell line, 16HBE, to copper and assessed the functional role of a circRNA, circ_0008882, by RNA overexpression. Cellular location of circ_0008882 was assessed by separation of nuclear and cytoplasmic RNAs. Nine circRNAs were associated with an increased risk for CRDs, while the relative expression of circ_0008882 was decreased after copper exposure in vitro and in vivo. Copper exposure stimulated 16HBE cells to release proinflammatory IL-6 and IL-8. The release of the cytokines was inhibited by overexpression of circ_0008882. These results suggest a role for circ_0008882 in the regulation of CRD associated inflammation following copper exposure.

Topics: Case-Control Studies; Chronic Disease; Copper; Cytokines; Humans; Interleukin-6; Interleukin-8; MicroRNAs; Pneumonia; Respiration Disorders; RNA; RNA, Circular

The purpose of this study is to investigate whether airborne exposure to endotoxins, hydrogen sulphide (H2S), and inhalable particles negatively impacts the respiratory system and inflammatory blood proteins in sewage plant and sewer net system workers and, further, to determine dose-response associations between exposure and health outcomes.. In total, 148 waste water workers (WWWs) from urban and rural sewage plants and the sewer net system participated. One hundred and twenty-one workers were exposed to sewage, 46 from sewage plants and 75 from the sewer net system. Twenty-seven workers were characterized as little or not exposed and served as an internal reference group. Personal inhalable samples were analysed for endotoxins (Limulus assay), particle dust (gravimetrically) and Salmonella and Yersinia spp. (polymerase chain reaction method, PCR). Levels of H2S were measured using personal electro chemical sensors. Intercellular adhesion molecule 1 (ICAM-1), interleukin 8 (IL-8), surfactant protein D (SP-D), club cell protein 16 (CC16), and macrophage inflammatory protein (MIP) were determined by enzyme-linked immunosorbent assay and C-reactive protein (CRP) by an HS-MicroCRP assay in blood samples.. Workers in sewage plants were exposed to significantly higher levels of endotoxins compared to workers in the sewer net system [median 55 EU m-3 (4-262 EU m-3) and median 27 EU m-3 (1-304 EU m-3), respectively]. The estimated H2S index showed higher values when working in the sewer net system [median 3.1 (0.5-78.1)] compared to workers at the sewage plants [median 1.3 (0.5-9.3)], and the most excessive exposure was collecting sewage from cesspools (273 p.p.m.). No viable airborne Salmonella and Yersinia spp. were detected. The exposed workers had significantly higher CRP compared to the referents [1.2 µg ml-1 (0.1-19.0 µg ml-1) and 0.8 µg ml-1 (0.1-5.0 µg ml-1), respectively] and lower forced expiratory volume in 1 s (FEV1)% [92.6%, standard deviation (SD) 14.6 and 102.0%, SD 10.1, respectively], with numbers given as mean and SD. The serum concentration of CRP was significantly and negatively associated with FEV1% (β = -7.7, R2 = 0.05) and forced vital capacity % (β = -8.5, R2 = 0.08), and the serum concentration of ICAM-1 with the estimated exposure to H2S (β = -19.9, R2 = 0.07).. Despite moderate levels of endotoxin and H2S exposure, the results indicate an impact of these agents on lung function and the adhesion molecule ICAM-1, and a low-grade systemic inflammation was indicated in increased levels of CRP.

Topics: Adult; Biomarkers; C-Reactive Protein; Dust; Endotoxins; Female; Humans; Hydrogen Sulfide; Intercellular Adhesion Molecule-1; Interleukin-8; Male; Middle Aged; Occupational Diseases; Occupational Exposure; Pulmonary Surfactant-Associated Protein D; Respiration Disorders; Respiratory System; Sewage; Wastewater

Several chronic respiratory diseases exhibit hyperactive immune responses in the lung: abundant inflammatory mediators; infiltrating neutrophils, macrophages, lymphocytes and other immune cells; and increased level of proteases. Such diseases include cystic fibrosis (CF), chronic obstructive pulmonary disease (COPD) and severe/neutrophilic asthma. Paradoxically, patients with these diseases are also susceptible to detrimental bacterial infection and colonization. In this paper, we seek to explain how a positive feedback mechanism via IL-8 could lead to desensitization of epithelial cells to pathogen recognition thus perpetuating bacterial colonization and chronic disease states in the lung. Such insight was obtained from mathematical modeling of the IRAK/TRAF6 signaling module, and is consistent with existing clinical evidence. The potential implications for targeted treatment regimes for these persistent respiratory diseases are explored.

Topics: Asthma; Epithelial Cells; Humans; Interleukin-1 Receptor-Associated Kinases; Interleukin-8; Lung; Models, Biological; Pulmonary Disease, Chronic Obstructive; Respiration Disorders; Signal Transduction; TNF Receptor-Associated Factor 6

The host inflammatory response and innate immunity play a complex role in respiratory diseases.. We evaluated the levels of inflammatory mediators and antibacterial proteins in children who required bronchoscopy and bronchoalveolar lavage fluid (BALF) for clinical indications such as chronic tracheostomy (n=15) and chronic suppurative lung disease (n=8).. Our results suggested the presence of interleukin-1beta (IL-1beta) and IL-8 as major inflammatory mediators in BALF samples. The level of the antibacterial protein sIgA was higher than lactoferrin and lysozyme. BALF IL-8 levels significantly correlated with the presence of IL-1beta, IL-6, IL-10, IL-16, sIgA and lysozyme. BALF IL-8 levels did not correlate with the levels of immunomodulatory and anti-inflammatory clara cell 10 kDa protein (CC10) or lactoferrin.. This study suggests that patients with high levels of BALF IL-8 could potentially have high levels of IL-6, IL-10, IL-16, lysozyme and sIgA. Evaluating the inflammatory mediators (IL-8) in relation to other BALF protein components provides insight into understanding the role of inflammatory mediators in the regulation of host defense and the response to lung inflammation and injury.

Topics: Biomarkers; Bronchiolitis; Bronchoalveolar Lavage; Bronchoalveolar Lavage Fluid; Bronchoscopy; Child; Humans; Immunity, Innate; Inflammation; Interleukin-1; Interleukin-8; Lactoferrin; Respiration Disorders; Uteroglobin

To compare respiratory symptoms and upper airway inflammation in domestic waste collectors and controls, and to find the association between measures of upper airway inflammation on the one hand and exposure concentrations of organic dust or respiratory symptoms on the other hand.. In a cross sectional study among 47 waste collectors and 15 controls, questionnaire data on respiratory symptoms were collected. Nasal lavage (NAL), to assess upper airway inflammation, was performed before and after a work shift at the beginning and at the end of the working week. In NAL fluid, cells were counted and differentiated and concentrations of interleukin 6 (IL6), IL8, tumour necrosis factor-alpha (TNF alpha), and IL1 beta were measured. In collectors, inhalable dust samples were collected in which bacterial endotoxin and mould beta(1-->3)-glucan were assessed.. Prevalence of respiratory symptoms was higher in waste collectors than in controls. Geometric mean exposure concentrations were 0.58 mg/m(3) for dust, 39 EU/m(3) for endotoxin, and 1.3 microg/m(3) for beta(1-->3)-glucan. At the end of the week collectors had higher concentrations of total cells and IL8 in NAL before and after a shift than controls (cells, before 1.9-fold p<0.10, after 3.3-fold p<0.01; IL8, before and after 1.8-fold p<0.05), and after/before work shift ratios of total cells were also higher (2.3-fold p=0.06) in collectors than in controls. Cells in NAL fluid consisted predominantly of neutrophils and epithelial cells, whereas eosinophils and mononuclear cells were rarely found. Exposure to dust and endotoxin was associated with concentrations of IL8 after the shift (p<0.05). Increased concentrations of IL8 (p<0.05) and total cells (p<0.10) after the shift were associated with respiratory symptoms. Concentrations of IL6, TNF alpha, and IL1 beta were not associated with waste collecting, symptoms, or exposure.. Waste collectors show signs of increased upper airway inflammation and respiratory symptoms compared with controls. Exposure to organic dust probably underlies the inflammation mediated by neutrophils that result in respiratory symptoms.

Topics: Adult; Cross-Sectional Studies; Dust; Humans; Interleukin-1; Interleukin-6; Interleukin-8; Male; Nasal Lavage Fluid; Netherlands; Occupational Diseases; Occupational Exposure; Refuse Disposal; Respiration Disorders; Respiratory Tract Diseases; Tumor Necrosis Factor-alpha; Waste Products