Quantification and role of innate lymphoid cell subsets in Chronic Obstructive Pulmonary Disease

التفاصيل البيبلوغرافية
العنوان: Quantification and role of innate lymphoid cell subsets in Chronic Obstructive Pulmonary Disease
المؤلفون: Fien M. Verhamme, Philip M. Hansbro, Evy E. Blomme, Hannelore Van Eeckhoutte, Guy Brusselle, Elise G De Smet, Joyceline De Volder, Marina Saetta, Sharen Provoost, Katrien De Grove, Matteo Bonato, Ken R. Bracke, Tania Maes, Sara R.A. Wijnant, Guy Joos
المساهمون: Epidemiology
المصدر: Clinical and Translational Immunology, 10(6):e1287. John Wiley & Sons Inc.
Clinical & Translational Immunology, Vol 10, Iss 6, Pp n/a-n/a (2021)
Clinical & Translational Immunology
CLINICAL & TRANSLATIONAL IMMUNOLOGY
سنة النشر: 2021
مصطلحات موضوعية: 0301 basic medicine, Immunology, Population, innate lymphoid cells, Inflammation, PHENOTYPE, 03 medical and health sciences, 0302 clinical medicine, Immune system, INFLAMMATION, Medicine and Health Sciences, IL-17A, medicine, 1107 Immunology, 1115 Pharmacology and Pharmaceutical Sciences, Immunology and Allergy, COPD, education, skin and connective tissue diseases, General Nursing, education.field_of_study, Lung, medicine.diagnostic_test, business.industry, Innate lymphoid cell, innate inflammation, GAMMA, RC581-607, Acquired immune system, medicine.disease, respiratory tract diseases, body regions, 030104 developmental biology, Bronchoalveolar lavage, medicine.anatomical_structure, 030228 respiratory system, ILC, Original Article, medicine.symptom, Immunologic diseases. Allergy, business
الوصف: Objectives 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.
In this article, we investigated the role of pulmonary innate lymphoid cells (ILCs) in the pathogenesis of chronic obstructive pulmonary disease (COPD). We found that the ILC1 subset is increased in COPD patients and correlates with smoking and severity of respiratory symptoms. In C57BL/6 mice, ILCs increase upon cigarette smoke (CS) exposure. In the absence of adaptive immunity, ILCs contribute to CS‐induced pro‐inflammatory mediator release, but they are redundant in CS‐induced innate inflammation.
وصف الملف: application/pdf; Electronic-eCollection
اللغة: English
تدمد: 2050-0068
URL الوصول: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::eb214b403e2eb61058534211f79749a2
https://pure.eur.nl/en/publications/c81cf8b6-50bd-465b-845a-15a6f26fc1a1
حقوق: OPEN
رقم الأكسشن: edsair.doi.dedup.....eb214b403e2eb61058534211f79749a2
قاعدة البيانات: OpenAIRE