دورية أكاديمية
أعرض في EDS

Chronic exposure of diesel exhaust particles induces alveolar enlargement in mice.

التفاصيل البيبلوغرافية
العنوان: Chronic exposure of diesel exhaust particles induces alveolar enlargement in mice.
المؤلفون: Yoshizaki K, Brito JM, Moriya HT, Toledo AC, Ferzilan S, Ligeiro de Oliveira AP, Machado ID, Farsky SH, Silva LF, Martins MA, Saldiva PH, Mauad T, Macchione M
المصدر: Respiratory research [Respir Res] 2015 Feb 07; Vol. 16, pp. 18. Date of Electronic Publication: 2015 Feb 07.
نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: BioMed Central Ltd Country of Publication: England NLM ID: 101090633 Publication Model: Electronic Cited Medium: Internet ISSN: 1465-993X (Electronic) Linking ISSN: 14659921 NLM ISO Abbreviation: Respir Res Subsets: MEDLINE
أسماء مطبوعة: Publication: 2001- : London : BioMed Central Ltd.
Original Publication: London : Current Science Ltd., c2000-
مواضيع طبية MeSH: Air Pollutants/*toxicity , Pneumonia/*chemically induced , Pulmonary Alveoli/*drug effects , Vehicle Emissions/*toxicity, Animals ; Brazil ; Bronchoalveolar Lavage Fluid/immunology ; Collagen/metabolism ; Cytokines/immunology ; Cytokines/metabolism ; Elastic Tissue/metabolism ; Inflammation Mediators/metabolism ; Lymphocyte Subsets/drug effects ; Lymphocyte Subsets/immunology ; Lymphocyte Subsets/metabolism ; Macrophages/drug effects ; Macrophages/immunology ; Macrophages/metabolism ; Male ; Mice, Inbred BALB C ; Mucin 5AC/genetics ; Mucin 5AC/metabolism ; Pneumonia/immunology ; Pneumonia/metabolism ; Pneumonia/pathology ; Pneumonia/physiopathology ; Pulmonary Alveoli/immunology ; Pulmonary Alveoli/metabolism ; Pulmonary Alveoli/pathology ; Pulmonary Alveoli/physiopathology ; RNA, Messenger/metabolism ; Respiratory Mechanics/drug effects ; Time Factors
مستخلص: Background: Diesel exhaust particles (DEPs) are deposited into the respiratory tract and are thought to be a risk factor for the development of diseases of the respiratory system. In healthy individuals, the timing and mechanisms of respiratory tract injuries caused by chronic exposure to air pollution remain to be clarified.
Methods: We evaluated the effects of chronic exposure to DEP at doses below those found in a typical bus corridor in Sao Paulo (150 μg/m3). Male BALB/c mice were divided into mice receiving a nasal instillation: saline (saline; n = 30) and 30 μg/10 μL of DEP (DEP; n = 30). Nasal instillations were performed five days a week, over a period of 90 days. Bronchoalveolar lavage (BAL) was performed, and the concentrations of interleukin (IL)-4, IL-10, IL-13 and interferon-gamma (INF-γ) were determined by ELISA-immunoassay. Assessment of respiratory mechanics was performed. The gene expression of Muc5ac in lung was evaluated by RT-PCR. The presence of IL-13, MAC2+ macrophages, CD3+, CD4+, CD8+ T cells and CD20+ B cells in tissues was analysed by immunohistochemistry. Bronchial thickness and the collagen/elastic fibers density were evaluated by morphometry. We measured the mean linear intercept (Lm), a measure of alveolar distension, and the mean airspace diameter (D0) and statistical distribution (D2).
Results: DEP decreased IFN-γ levels in BAL (p = 0.03), but did not significantly alter IL-4, IL-10 and IL-13 levels. MAC2+ macrophage, CD4+ T cell and CD20+ B cell numbers were not altered; however, numbers of CD3+ T cells (p ≤ 0.001) and CD8+ T cells (p ≤ 0.001) increased in the parenchyma. Although IL-13 (p = 0.008) expression decreased in the bronchiolar epithelium, Muc5ac gene expression was not altered in the lung of DEP-exposed animals. Although respiratory mechanics, elastic and collagen density were not modified, the mean linear intercept (Lm) was increased in the DEP-exposed animals (p ≤ 0.001), and the index D2 was statistically different (p = 0.038) from the control animals.
Conclusion: Our data suggest that nasal instillation of low doses of DEP over a period of 90 days results in alveolar enlargement in the pulmonary parenchyma of healthy mice.
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المشرفين على المادة: 0 (Air Pollutants)
0 (Cytokines)
0 (Inflammation Mediators)
0 (Muc5ac protein, mouse)
0 (Mucin 5AC)
0 (RNA, Messenger)
0 (Vehicle Emissions)
9007-34-5 (Collagen)
تواريخ الأحداث: Date Created: 20150408 Date Completed: 20160329 Latest Revision: 20181113
رمز التحديث: 20231215
مُعرف محوري في PubMed: PMC4345004
DOI: 10.1186/s12931-015-0172-z
PMID: 25848680
قاعدة البيانات: MEDLINE
الوصف
تدمد:1465-993X
DOI:10.1186/s12931-015-0172-z