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  • 1
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    Mendelian Randomization Study of Interleukin-6 in Chronic Obstructive Pulmonary Disease
    S. Karger AG ; 2011
    In:  Respiration Vol. 82, No. 6 ( 2011), p. 530-538
    Details
    In: Respiration, S. Karger AG, Vol. 82, No. 6 ( 2011), p. 530-538
    Abstract: 〈 i 〉 Background: 〈 /i 〉 Cross-sectional studies have demonstrated that increased levels of interleukin-6 (IL6) are present in the airways and blood samples of patients with chronic obstructive pulmonary disease (COPD). 〈 i 〉 Objectives: 〈 /i 〉 To investigate the association between IL6 and the risk of COPD using a Mendelian randomization approach. 〈 i 〉 Methods: 〈 /i 〉 Eight common single-nucleotide polymorphisms (SNPs) in the region of the 〈 i 〉 IL6 〈 /i 〉 gene were genotyped using both TaqMan and Illumina in the Rotterdam Study, a prospective population-based cohort study consisting of 7,983 participants aged 55 years or older, including 928 COPD patients. At baseline, blood was drawn in a random sample of 714 subjects to measure the IL6 plasma level. Analysis of variance, logistic regression, and Cox proportional hazard models – adjusted for age, gender, pack years, and BMI – were used for analyses. 〈 i 〉 Results: 〈 /i 〉 High levels of IL6 ( 〉 2.4 pg/ml, the highest tertile) were associated with a three-fold increased risk of developing COPD, in comparison to low levels ( 〈 1.4 pg/ml, the lowest tertile). The rs2056576 SNP was associated with a 10% increase in the risk of COPD per additional T allele. However, the association was no longer significant after adjustment. No association was found with other common SNPs in the 〈 i 〉 IL6 〈 /i 〉 gene and COPD. 〈 i 〉 Conclusions: 〈 /i 〉 Although increased IL6 plasma levels at baseline are associated with the risk of developing COPD during follow-up, there was no strong evidence for an association between common variation in the 〈 i 〉 IL6 〈 /i 〉 gene and the risk of COPD.
    Type of Medium: Online Resource
    ISSN: 0025-7931 , 1423-0356
    URL: Article
    DOI: 10.1159/000332336
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2011
    detail.hit.zdb_id: 1464419-8
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  • 2
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    Innate lymphoid cells in isocyanate-induced asthma: role of microRNA-155
    European Respiratory Society (ERS) ; 2020
    In:  European Respiratory Journal Vol. 56, No. 3 ( 2020-09), p. 1901289-
    Details
    In: European Respiratory Journal, European Respiratory Society (ERS), Vol. 56, No. 3 ( 2020-09), p. 1901289-
    Abstract: Occupational asthma, induced by workplace exposures to low molecular weight agents such as toluene 2,4-diisocyanate (TDI), causes a significant burden to patients and society. Little is known about innate lymphoid cells (ILCs) in TDI-induced asthma. A critical regulator of ILC function is microRNA-155, a microRNA associated with asthma. Objective To determine whether TDI exposure modifies the number of ILCs in the lung and whether microRNA-155 contributes to TDI-induced airway inflammation and hyperresponsiveness. Methods C57BL/6 wild-type and microRNA-155 knockout mice were sensitised and challenged with TDI or vehicle. Intracellular cytokine expression in ILCs and T-cells was evaluated in bronchoalveolar lavage (BAL) fluid using flow cytometry. Peribronchial eosinophilia and goblet cells were evaluated on lung tissue, and airway hyperresponsiveness was measured using the forced oscillation technique. Putative type 2 ILCs (ILC2) were identified in bronchial biopsies of subjects with TDI-induced occupational asthma using immunohistochemistry. Human bronchial epithelial cells were exposed to TDI or vehicle. Results TDI-exposed mice had higher numbers of airway goblet cells, BAL eosinophils, CD4 + T-cells and ILCs, with a predominant type 2 response, and tended to have airway hyperresponsiveness. In TDI-exposed microRNA-155 knockout mice, inflammation and airway hyperresponsiveness were attenuated. TDI exposure induced IL-33 expression in human bronchial epithelial cells and in murine lungs, which was microRNA-155 dependent in mice. GATA3 + CD3 − cells, presumably ILC2, were present in bronchial biopsies. Conclusion TDI exposure is associated with increased numbers of ILCs. The proinflammatory microRNA-155 is crucial in a murine model of TDI asthma, suggesting its involvement in the pathogenesis of occupational asthma due to low molecular weight agents.
    Type of Medium: Online Resource
    ISSN: 0903-1936 , 1399-3003
    URL: Article
    URL: Article
    URL: Article
    DOI: 10.1183/13993003.01289-2019
    DOI: 10.1183/13993003.01289-2019.Supp1
    DOI: 10.1183/13993003.01289-2019.Shareable1
    Language: English
    Publisher: European Respiratory Society (ERS)
    Publication Date: 2020
    detail.hit.zdb_id: 2834928-3
    detail.hit.zdb_id: 1499101-9
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  • 3
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    Risk of Frailty in Elderly With COPD: A Population-Based Study
    Oxford University Press (OUP) ; 2016
    In:  The Journals of Gerontology Series A: Biological Sciences and Medical Sciences Vol. 71, No. 5 ( 2016-05), p. 689-695
    Details
    In: The Journals of Gerontology Series A: Biological Sciences and Medical Sciences, Oxford University Press (OUP), Vol. 71, No. 5 ( 2016-05), p. 689-695
    Type of Medium: Online Resource
    ISSN: 1079-5006 , 1758-535X
    URL: Article
    DOI: 10.1093/gerona/glv154
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2016
    detail.hit.zdb_id: 2043927-1
    SSG: 12
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  • 4
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    Pro- and Anti-Inflammatory Role of ChemR23 Signaling in Pollutant-Induced Inflammatory Lung Responses
    The American Association of Immunologists ; 2016
    In:  The Journal of Immunology Vol. 196, No. 4 ( 2016-02-15), p. 1882-1890
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 196, No. 4 ( 2016-02-15), p. 1882-1890
    Abstract: Inhalation of traffic-related particulate matter (e.g., diesel exhaust particles [DEPs]) is associated with acute inflammatory responses in the lung, and it promotes the development and aggravation of allergic airway diseases. We previously demonstrated that exposure to DEP was associated with increased recruitment and maturation of monocytes and conventional dendritic cells (DCs), resulting in TH2 polarization. Monocytes and immature DCs express the G-protein coupled receptor chemR23, which binds the chemoattractant chemerin. Using chemR23 knockout (KO) and corresponding wild-type (WT) mice, we determined the role of chemR23 signaling in response to acute exposure to DEPs and in response to DEP-enhanced house dust mite (HDM)-induced allergic airway inflammation. Exposure to DEP alone, as well as combined exposure to DEP plus HDM, elevated the levels of chemerin in the bronchoalveolar lavage fluid of WT mice. In response to acute exposure to DEPs, monocytes and monocyte-derived DCs accumulated in the lungs of WT mice, but this response was significantly attenuated in chemR23 KO mice. Concomitant exposure to DEP plus HDM resulted in allergic airway inflammation with increased eosinophilia, goblet cell metaplasia, and TH2 cytokine production in WT mice, which was further enhanced in chemR23 KO mice. In conclusion, we demonstrated an opposing role for chemR23 signaling depending on the context of DEP-induced inflammation. The chemR23 axis showed proinflammatory properties in a model of DEP-induced acute lung inflammation, in contrast to anti-inflammatory effects in a model of DEP-enhanced allergic airway inflammation.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.1501113
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2016
    detail.hit.zdb_id: 1475085-5
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  • 5
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    Cigarette smoke exposure facilitates allergic sensitization in mice
    Springer Science and Business Media LLC ; 2006
    In:  Respiratory Research Vol. 7, No. 1 ( 2006-12)
    Details
    In: Respiratory Research, Springer Science and Business Media LLC, Vol. 7, No. 1 ( 2006-12)
    Abstract: Active and passive smoking are considered as risk factors for asthma development. The mechanisms involved are currently unexplained. Objective The aim of this study was to determine if cigarette smoke exposure could facilitate primary allergic sensitization. Methods BALB/c mice were exposed to aerosolized ovalbumin (OVA) combined with air or tobacco smoke (4 exposures/day) daily for three weeks. Serology, lung cytopathology, cytokine profiles in bronchoalveolar lavage fluid (BALF) and on mediastinal lymph node cultures as well as lung function tests were performed after the last exposure. The natural history and the immune memory of allergic sensitization were studied with in vivo recall experiments. Results Exposure to OVA induced a small increase in OVA-specific serum IgE as compared with exposure to PBS (P 〈 0.05), while no inflammatory reaction was observed in the airways. Exposure to cigarette smoke did not induce IgE, but was characterized by a small but significant neutrophilic inflammatory reaction. Combining OVA with cigarette smoke not only induced a significant increase in OVA-specific IgE but also a distinct eosinophil and goblet cell enriched airway inflammation albeit that airway hyperresponsiveness was not evidenced. FACS analysis showed in these mice increases in dendritic cells (DC) and CD4 + T-lymphocytes along with a marked increase in IL-5 measured in the supernatant of lymph node cell cultures. Immune memory experiments evidenced the transient nature of these phenomena. Conclusion In this study we show that mainstream cigarette smoke temporary disrupts the normal lung homeostatic tolerance to innocuous inhaled allergens, thereby inducing primary allergic sensitization. This is characterized not only by the development of persistent IgE, but also by the emergence of an eosinophil rich pulmonary inflammatory reaction.
    Type of Medium: Online Resource
    ISSN: 1465-993X
    URL: Article
    DOI: 10.1186/1465-9921-7-49
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2006
    detail.hit.zdb_id: 2041675-1
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  • 6
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    Quantification and role of innate lymphoid cell subsets in Chronic Obstructive Pulmonary Disease
    Wiley ; 2021
    In:  Clinical & Translational Immunology Vol. 10, No. 6 ( 2021-01)
    Details
    In: Clinical & Translational Immunology, Wiley, Vol. 10, No. 6 ( 2021-01)
    Abstract: Innate lymphoid cells (ILCs) secrete cytokines, such as IFN‐γ, IL‐13 and IL‐17, which are linked to chronic obstructive pulmonary disease (COPD). Here, we investigated the role of pulmonary ILCs in COPD pathogenesis. Methods Lung ILC subsets in COPD and control subjects were quantified using flow cytometry and associated with clinical parameters. Tissue localisation of ILC and T‐cell subsets was determined by immunohistochemistry. Mice were exposed to air or cigarette smoke (CS) for 1, 4 or 24 weeks to investigate whether pulmonary ILC numbers and activation are altered and whether they contribute to CS‐induced innate inflammatory responses. Results Quantification of lung ILC subsets demonstrated that ILC1 frequency in the total ILC population was elevated in COPD and was associated with smoking and severity of respiratory symptoms (COPD Assessment Test [CAT] score). All three ILC subsets localised near lymphoid aggregates in COPD. In the COPD mouse model, CS exposure in C57BL/6J mice increased ILC numbers at all time points, with relative increases in ILC1 in bronchoalveolar lavage (BAL) fluid. Importantly, CS exposure induced increases in neutrophils, monocytes and dendritic cells that remained elevated in Rag2 / Il2rg ‐deficient mice that lack adaptive immune cells and ILCs. However, CS‐induced CXCL1, IL‐6, TNF‐α and IFN‐γ levels were reduced by ILC deficiency. Conclusion The ILC1 subset is increased in COPD patients and correlates with smoking and severity of respiratory symptoms. ILCs also increase upon CS exposure in C57BL/6J mice. In the absence of adaptive immunity, ILCs contribute to CS‐induced pro‐inflammatory mediator release, but are redundant in CS‐induced innate inflammation.
    Type of Medium: Online Resource
    ISSN: 2050-0068 , 2050-0068
    URL: Issue
    URL: Article
    DOI: 10.1002/cti2.v10.6
    DOI: 10.1002/cti2.1287
    Language: English
    Publisher: Wiley
    Publication Date: 2021
    detail.hit.zdb_id: 2694482-0
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  • 7
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    RIPK1 kinase-dependent inflammation and cell death contribute to the pathogenesis of COPD
    European Respiratory Society (ERS) ; 2023
    In:  European Respiratory Journal Vol. 61, No. 4 ( 2023-04), p. 2201506-
    Details
    In: European Respiratory Journal, European Respiratory Society (ERS), Vol. 61, No. 4 ( 2023-04), p. 2201506-
    Abstract: Receptor-interacting protein kinase 1 (RIPK1) is a key mediator of regulated cell death (including apoptosis and necroptosis) and inflammation, both drivers of COPD pathogenesis. We aimed to define the contribution of RIPK1 kinase-dependent cell death and inflammation in the pathogenesis of COPD. Methods We assessed RIPK1 expression in single-cell RNA sequencing (RNA-seq) data from human and mouse lungs, and validated RIPK1 levels in lung tissue of COPD patients via immunohistochemistry. Next, we assessed the consequences of genetic and pharmacological inhibition of RIPK1 kinase activity in experimental COPD, using Ripk1 S25D/S25D kinase-deficient mice and the RIPK1 kinase inhibitor GSK′547. Results RIPK1 expression increased in alveolar type 1 (AT1), AT2, ciliated and neuroendocrine cells in human COPD. RIPK1 protein levels were significantly increased in airway epithelium of COPD patients compared with never-smokers and smokers without airflow limitation. In mice, exposure to cigarette smoke (CS) increased Ripk1 expression similarly in AT2 cells, and further in alveolar macrophages and T-cells. Genetic and/or pharmacological inhibition of RIPK1 kinase activity significantly attenuated airway inflammation upon acute and subacute CS exposure, as well as airway remodelling, emphysema, and apoptotic and necroptotic cell death upon chronic CS exposure. Similarly, pharmacological RIPK1 kinase inhibition significantly attenuated elastase-induced emphysema and lung function decline. Finally, RNA-seq on lung tissue of CS-exposed mice revealed downregulation of cell death and inflammatory pathways upon pharmacological RIPK1 kinase inhibition. Conclusions RIPK1 kinase inhibition is protective in experimental models of COPD and may represent a novel promising therapeutic approach.
    Type of Medium: Online Resource
    ISSN: 0903-1936 , 1399-3003
    URL: Article
    URL: Article
    URL: Article
    DOI: 10.1183/13993003.01506-2022
    DOI: 10.1183/13993003.01506-2022.Supp1
    DOI: 10.1183/13993003.01506-2022.Shareable1
    Language: English
    Publisher: European Respiratory Society (ERS)
    Publication Date: 2023
    detail.hit.zdb_id: 2834928-3
    detail.hit.zdb_id: 1499101-9
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  • 8
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    Cigarette smoke-induced pulmonary emphysema in scid-mice. Is the acquired immune system required?
    Springer Science and Business Media LLC ; 2005
    In:  Respiratory Research Vol. 6, No. 1 ( 2005-12)
    Details
    In: Respiratory Research, Springer Science and Business Media LLC, Vol. 6, No. 1 ( 2005-12)
    Abstract: Chronic obstructive pulmonary disease is associated with a chronic inflammatory response of the host to chronic exposure to inhaled toxic gases and particles. Although inflammatory cells of both the innate and adaptive immune system infiltrate the lungs in pulmonary emphysema and form lymphoid follicles around the small airways, the exact role of the acquired immune system in the pathogenesis of emphysema is not known. Methods In this study, wild type Balb/c mice and immunodeficient scid mice – which lack functional B- and T-cells – were exposed to mainstream cigarette smoke (CS) for 5 weeks or 6 months. Results Subacute CS-exposure for 5 weeks significantly increased innate inflammatory cells (neutrophils, macrophages and dendritic cells) in the bronchoalveolar lavage (BAL) fluid of wild type mice and scid mice, which correlated with the CS-induced upregulation of the chemokines Monocyte Chemotactic Protein-1, Macrophage Inflammatory Protein-3α and KC (= mouse Interleukin-8). Chronic CS-exposure for 6 months significantly increased the number of neutrophils, macrophages, dendritic cells, CD4 + and CD8 + T-lymphocytes in BAL fluid and lungs of wild type mice compared to air-exposed littermates, and augmented the size and number of peribronchial lymphoid follicles. In contrast, neither B-lymphocytes, nor T-lymphocytes, nor lymphoid follicles could be discerned in the lungs of air- or CS-exposed scid mice. Importantly, chronic CS-exposure induced pulmonary emphysema in both wild type animals and scid mice, as evidenced by a significant increase in the mean linear intercept and the destructive index of CS-exposed versus air-exposed animals. The CS-induced emphysema was associated with increased mRNA expression of matrix metalloproteinase-12 in the lungs and increased protein levels of Tumor Necrosis Factor-α in the BAL fluid of CS-exposed Balb/c and scid mice compared to air-exposed littermates. Conclusion This study suggests that the adaptive immune system is not required per se to develop pulmonary emphysema in response to chronic CS-exposure, since emphysema can be induced in scid mice, which lack lymphoid follicles as well as functional B- and T-cells.
    Type of Medium: Online Resource
    ISSN: 1465-993X
    URL: Article
    DOI: 10.1186/1465-9921-6-147
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2005
    detail.hit.zdb_id: 2041675-1
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  • 9
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    Statins, systemic inflammation and risk of death in COPD: The Rotterdam study
    Elsevier BV ; 2013
    In:  Pulmonary Pharmacology & Therapeutics Vol. 26, No. 2 ( 2013-4), p. 212-217
    Details
    In: Pulmonary Pharmacology & Therapeutics, Elsevier BV, Vol. 26, No. 2 ( 2013-4), p. 212-217
    Type of Medium: Online Resource
    ISSN: 1094-5539
    URL: Article
    DOI: 10.1016/j.pupt.2012.10.008
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2013
    detail.hit.zdb_id: 1471690-2
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  • 10
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    C-Reactive Protein Levels, Haplotypes, and the Risk of Incident Chronic Obstructive Pulmonary Disease
    American Thoracic Society ; 2009
    In:  American Journal of Respiratory and Critical Care Medicine Vol. 179, No. 5 ( 2009-03-01), p. 375-382
    Details
    In: American Journal of Respiratory and Critical Care Medicine, American Thoracic Society, Vol. 179, No. 5 ( 2009-03-01), p. 375-382
    Type of Medium: Online Resource
    ISSN: 1073-449X , 1535-4970
    URL: Article
    DOI: 10.1164/rccm.200810-1540OC
    RVK:
    XA 21200
    Language: English
    Publisher: American Thoracic Society
    Publication Date: 2009
    detail.hit.zdb_id: 1468352-0
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