دورية أكاديمية
أعرض في EDS

Chronic exposure to diesel particles worsened emphysema and increased M2-like phenotype macrophages in a PPE-induced model.

التفاصيل البيبلوغرافية
العنوان: Chronic exposure to diesel particles worsened emphysema and increased M2-like phenotype macrophages in a PPE-induced model.
المؤلفون: Moreira AR; Department of Clinical Medicine (LIM 20), School of Medicine, University of Sao Paulo, Sao Paulo, Brazil., Pereira de Castro TB; Institute of Medical Assistance to the State Public Servant (IAMSPE), Sao Paulo, Brazil.; University City of Sao Paulo (UNICID), Sao Paulo, Brazil., Kohler JB; Department of Clinical Medicine (LIM 20), School of Medicine, University of Sao Paulo, Sao Paulo, Brazil., Ito JT; Department of Clinical Medicine (LIM 20), School of Medicine, University of Sao Paulo, Sao Paulo, Brazil., de França Silva LE; Department of Clinical Medicine (LIM 20), School of Medicine, University of Sao Paulo, Sao Paulo, Brazil., Lourenço JD; Department of Clinical Medicine (LIM 20), School of Medicine, University of Sao Paulo, Sao Paulo, Brazil., Almeida RR; Department of Immunology, Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo, Brazil.; Heart Institute (InCor) School of Medicine, University of Sao Paulo, Sao Paulo, Brazil., Santana FR; Department of Bioscience, Federal University of Sao Paulo, Diadema, Sao Paulo, Brazil., Brito JM; Department of Pathology (LIM 5), School of Medicine, University of Sao Paulo, Sao Paulo, Brazil., Rivero DHRF; Department of Pathology (LIM 5), School of Medicine, University of Sao Paulo, Sao Paulo, Brazil., Vale MICA; Department of Bioscience, Federal University of Sao Paulo, Diadema, Sao Paulo, Brazil., Prado CM; Department of Bioscience, Federal University of Sao Paulo, Santos, Sao Paulo, Brazil., Câmara NOS; Department of Immunology, Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo, Brazil.; Department of Clinical Medicine (LIM 16), School of Medicine, University of Sao Paulo, Sao Paulo, Brazil.; Department of Medicine, Nephrology Division, Federal University of Sao Paulo, Sao Paulo, Brazil., Saldiva PHN; Department of Pathology (LIM 5), School of Medicine, University of Sao Paulo, Sao Paulo, Brazil., Olivo CR; Department of Clinical Medicine (LIM 20), School of Medicine, University of Sao Paulo, Sao Paulo, Brazil.; Institute of Medical Assistance to the State Public Servant (IAMSPE), Sao Paulo, Brazil.; University City of Sao Paulo (UNICID), Sao Paulo, Brazil., Lopes FDTQDS; Department of Clinical Medicine (LIM 20), School of Medicine, University of Sao Paulo, Sao Paulo, Brazil.
المصدر: PloS one [PLoS One] 2020 Jan 31; Vol. 15 (1), pp. e0228393. Date of Electronic Publication: 2020 Jan 31 (Print Publication: 2020).
نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: Public Library of Science Country of Publication: United States NLM ID: 101285081 Publication Model: eCollection Cited Medium: Internet ISSN: 1932-6203 (Electronic) Linking ISSN: 19326203 NLM ISO Abbreviation: PLoS One Subsets: MEDLINE
أسماء مطبوعة: Original Publication: San Francisco, CA : Public Library of Science
مواضيع طبية MeSH: Air Pollutants/*toxicity , Macrophages/*metabolism , Pancreatic Elastase/*adverse effects , Pulmonary Emphysema/*immunology , Vehicle Emissions/*toxicity, Administration, Intranasal ; Animals ; Apoptosis ; Bronchoalveolar Lavage Fluid/immunology ; Case-Control Studies ; Disease Models, Animal ; Male ; Mice ; Mice, Inbred C57BL ; Pancreatic Elastase/administration & dosage ; Pulmonary Emphysema/chemically induced
مستخلص: Chronic exposure to ambient levels of air pollution induces respiratory illness exacerbation by increasing inflammatory responses and apoptotic cells in pulmonary tissues. The ineffective phagocytosis of these apoptotic cells (efferocytosis) by macrophages has been considered an important factor in these pathological mechanisms. Depending on microenvironmental stimuli, macrophages can assume different phenotypes with different functional actions. M1 macrophages are recognized by their proinflammatory activity, whereas M2 macrophages play pivotal roles in responding to microorganisms and in efferocytosis to avoid the progression of inflammatory conditions. To verify how exposure to air pollutants interferes with macrophage polarization in emphysema development, we evaluated the different macrophage phenotypes in a PPE- induced model with the exposure to diesel exhaust particles. C57BL/6 mice received intranasal instillation of porcine pancreatic elastase (PPE) to induce emphysema, and the control groups received saline. Both groups were exposed to diesel exhaust particles or filtered air for 60 days according to the groups. We observed that both the diesel and PPE groups had an increase in alveolar enlargement, collagen and elastic fibers in the parenchyma and the number of macrophages, lymphocytes and epithelial cells in BAL, and these responses were exacerbated in animals that received PPE instillation prior to exposure to diesel exhaust particles. The same response pattern was found inCaspase-3 positive cell analysis, attesting to an increase in cell apoptosis, which is in agreement with the increase in M2 phenotype markers, measured by RT-PCR and flow cytometry analysis. We did not verify differences among the groups for the M1 phenotype. In conclusion, our results showed that both chronic exposure to diesel exhaust particles and PPE instillation induced inflammatory conditions, cell apoptosis and emphysema development, as well as an increase in M2 phenotype macrophages, and the combination of these two factors exacerbated these responses. The predominance of the M2-like phenotype likely occurred due to the increased demand for efferocytosis. However, M2 macrophage activity was ineffective, resulting in emphysema development and worsening of symptoms.
Competing Interests: The authors have declared that no competing interests exist.
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المشرفين على المادة: 0 (Air Pollutants)
0 (Vehicle Emissions)
EC 3.4.21.36 (Pancreatic Elastase)
تواريخ الأحداث: Date Created: 20200201 Date Completed: 20200417 Latest Revision: 20240725
رمز التحديث: 20240726
مُعرف محوري في PubMed: PMC6993960
DOI: 10.1371/journal.pone.0228393
PMID: 32004356
قاعدة البيانات: MEDLINE
الوصف
تدمد:1932-6203
DOI:10.1371/journal.pone.0228393