Academic Journal
Cigarette smoking induces human CCR6+Th17 lymphocytes senescence and VEGF-A secretion
| العنوان: | Cigarette smoking induces human CCR6+Th17 lymphocytes senescence and VEGF-A secretion |
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| المؤلفون: | Baskara, Indoumady, Kerbrat, Stéphane, Dagouassat, Maylis, Nguyen, Hoang Quy, Guillot-Delost, Maude, Surénaud, Mathieu, Baillou, Claude, Lemoine, François, M, Morin, Didier, Boczkowski, Jorge, Le Gouvello, Sabine |
| المساهمون: | Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12), IMRB - GEIC2O/"Genetic and Environmental Interactions in COPD, Cystic fibrosis and Other (rare) respiratory diseases" Créteil (U955 Inserm - UPEC), Institut Mondor de Recherche Biomédicale (IMRB), Institut National de la Santé et de la Recherche Médicale (INSERM)-IFR10-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12)-Institut National de la Santé et de la Recherche Médicale (INSERM)-IFR10-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12), Recherche Translationnelle en Oncogénèse Génito-Urinaire Equipe 7 (Inserm U955 - IMRB - UPEC), Institut Curie Paris, Immunité et cancer (U932), Institut Curie Paris -Institut National de la Santé et de la Recherche Médicale (INSERM), IMRB - "From pathophysiology towards immune-basedinterventions in HIV infection" Créteil (U955 Inserm - UPEC), Centre d'Immunologie et des Maladies Infectieuses (CIMI), Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS), IMRB - PROTECT/"Pharmacologie et Technologies pour les Maladies Cardiovasculaires" Créteil (U955 Inserm - UPEC), Pôle de Biologie-Pathologie Créteil, Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Henri Mondor-Hôpital Albert Chenevier, This work was supported by the Institut National de la Santé et de la Recherche Médicale, by the Leg Poix, and by private donators. I. Baskara was supported by a PhD scholarship from the Fondation de Recherche en Santé Respiratoire/Fondation du Souffle. |
| المصدر: | ISSN: 2045-2322. |
| بيانات النشر: | CCSD Nature Publishing Group |
| سنة النشر: | 2020 |
| مصطلحات موضوعية: | [SDV.BC]Life Sciences [q-bio]/Cellular Biology, [SDV.MHEP.PSR]Life Sciences [q-bio]/Human health and pathology/Pulmonology and respiratory tract |
| الوصف: | International audience ; Chronic exposure to environmental pollutants is often associated with systemic inflammation. As such, cigarette smoking contributes to inflammation and lung diseases by inducing senescence of pulmonary cells such as pneumocytes, fibroblasts, and endothelial cells. Yet, how smoking worsens evolution of chronic inflammatory disorders associated with Th17 lymphocytes, such as rheumatoid arthritis, psoriasis, Crohn's disease, and multiple sclerosis, is largely unknown. Results from human studies show an increase in inflammatory CD4+ Th17 lymphocytes at blood- and pulmonary level in smokers. The aim of the study was to evaluate the sensitivity of CD4+ Th17 lymphocytes to cigarette smoke-induced senescence. Mucosa-homing CCR6+ Th17- were compared to CCR6neg -and regulatory T peripheral lymphocytes after exposure to cigarette smoke extract (CSE). Senescence sensitivity of CSE-exposed cells was assessed by determination of various senescence biomarkers (β-galactosidase activity, p16Ink4a- and p21 expression) and cytokines production. CCR6+ Th17 cells showed a higher sensitivity to CSE-induced senescence compared to controls, which is associated to oxidative stress and higher VEGFα secretion. Pharmacological targeting of ROS- and ERK1/2 signalling pathways prevented CSE-induced senescence of CCR6+Th17 lymphocytes as well as VEGFα secretion. Altogether, these results identify mechanisms by which pro-oxidant environmental pollutants contribute to pro-angiogenic and pathogenic CCR6+Th17 cells, therefore potential targets for therapeutic purposes. |
| نوع الوثيقة: | article in journal/newspaper |
| اللغة: | English |
| Relation: | info:eu-repo/semantics/altIdentifier/pmid/32300208; PUBMED: 32300208; PUBMEDCENTRAL: PMC7162978 |
| DOI: | 10.1038/s41598-020-63613-4 |
| الاتاحة: | https://inserm.hal.science/inserm-02874018 https://inserm.hal.science/inserm-02874018v1/document https://inserm.hal.science/inserm-02874018v1/file/s41598-020-63613-4.pdf https://doi.org/10.1038/s41598-020-63613-4 |
| Rights: | info:eu-repo/semantics/OpenAccess |
| رقم الانضمام: | edsbas.AFF69C52 |
| قاعدة البيانات: | BASE |
| DOI: | 10.1038/s41598-020-63613-4 |
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