Author of

• 28971

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  Lunch & Poster Display session (ID 58)

  • Event: ELCC 2019
  • Type: Poster Display session
  • Track:
  • Presentations: 1
  • Moderators:
  • Coordinates: 4/11/2019, 12:30 - 13:00, Hall 1

  • 28988

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    20P - Atypical hyperplasia of bronchial epithelial cells induced by chronic exposure to PM 2.5 in mice (ID 301)

    12:30 - 13:00  |  Presenting Author(s): Tian Fang Hou
    • Abstract

    Background
    

    Air pollution is still a major environmental problem affecting the health of the respiratory system. Studies have confirmed that air pollution is closely related to the occurrence of lung cancer. Air pollution (mainly PM2.5) has been classified as a carcinogen by the International Agency for Research on Cancer. Previous evidence of the relationship between PM2.5 and lung cancer mostly comes from countries with low PM2.5 exposure level. Exposure to fine particulate matter (PM2.5) may increase the risk of lung cancer, but the underlying mechanism is still unclear.There is no direct evidence that PM2.5 can directly induce lung cancer .The aim of our study was to investigate the atypical hyperplasia of bronchial epithelial cells induced by chronic exposure to PM2.5 in mice and the possible mechanism of PM2.5 in the pathogenesis of severe atypical hyperplasia.

    a9ded1e5ce5d75814730bb4caaf49419 Methods
    

    30 BALB/c mice were treated with noninvasive tracheal instillation of PM2.5 suspension at different doses (2.5mg/kg, 5mg/kg, 10mg/kg) for 90 days (one time every 3 days), and the blank group and saline group were set as a control group. Tissue samples were taken at the end of the endotracheal infusion. Histopathological changes of lung tissue in mice and the expression of TTF-1, CK7 and Ki67 were detected by Hematoxylin-Eosin staining and immunohistochemical staining respectively.

    20c51b5f4e9aeb5334c90ff072e6f928 Results
    

    Histopathological changes showed atypical hyperplasia of bronchiolo epithelia, part of glands papillary hyperplasia, some luminal glands crowded and disordered, glandular cavity back-to-back phenomenon, pulmonary septum widened, alveolar macrophages with engulfed particles and lymphocyte aggregation in bronchiole and alveolar, especially at high dose exposure group. Electron microscopic observation showed that normal structure of alveolar and bronchial epithelial cells disappeared and a large number of autophagic bodies were formed in the alveolar and bronchial epithelial cells of mice. The expression of TTF-1, CK7 and Ki67 in the lung tissue with 10mg/kg PM2.5 were positive.

    fd69c5cf902969e6fb71d043085ddee6 Conclusions
    

    Chronic exposure to PM2.5 induced severe atypical hyperplasia of the bronchial epithelial cells in mice, it suggested that the model of severe atypical hyperplasia of lung in mice was established.

    b651e8a99c4375feb982b7c2cad376e9 Legal entity responsible for the study
    

    The authors.

    213f68309caaa4ccc14d5f99789640ad Funding
    

    Has not received any funding.

    682889d0a1d3b50267a69346a750433d Disclosure
    

    All authors have declared no conflicts of interest.

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