Premium
Disorder of Renin‐Angiotensin System Promoting the Acute Pulmonary Inflammation by Particulate Matter 2.5 (PM 2.5 ) Exposure
Author(s) -
Lin ChungI,
Wang GuanHua,
Cho ChingChang,
Wu Hsi Tien,
Hsieh WenYeh,
Lin ChihSheng
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.854.6
Subject(s) - inflammation , lung , oxidative stress , chemistry , particulates , renin–angiotensin system , medicine , pathology , endocrinology , immunology , blood pressure , organic chemistry
Acute or chronic particulate matter 2.5 (PM 2.5 ) exposure can induce oxidative stress, inflammation and pulmonary impairment by traversing the blood‐air barrier of alveolar and then depositing at lung. In the present study, we tested whether the pulmonary inflammation and impairment induced by PM 2.5 exposure are related to the disorder of pulmonary renin‐angiotensin system (RAS). In this study, we collected PM 2.5 from waste gas which was produced from vehicle engine, and determined the component elements and structures of the PM 2.5 . The C57BL/6J (wild type, WT) mice and angiotensin converting enzyme II (ACE2) gene knockout (ACE2KO) mice were treated with the PM 2.5 by intratracheal instillation once a day for a total of 3 days, and then sacrificed at the 4th day. Lung tissue of the mice was collected for the assays of molecular, biochemical and pathological changes to evaluate the acute pulmonary inflammation and lung injury induced by PM 2.5 exposure. The results indicated that the most of collected particulates in this study were aggregated and parts of them formed structure of chains below 2.5 μm diameter. The major compositions of the PM 2.5 are carbon and oxide, and contain little silicon, sulfate and copper. The body weight of both WT and ACE2 KO mice treated with PM 2.5 was decreased and resting breathing rate was significantly increased. PM 2.5 treatment induced pathological leukocyte infiltration in the lung, increased pulmonary immunocytokines concentration, including interleukin‐6 (IL‐6), tumor necrosis factor alpha (TNF‐α) and tumor growth factor beta 1 (TGF‐β1), and also promoted signaling protein ERK1/2 and STAT3 phosphorylation. The quantitative data showed that the levels of physiopathology and inflammation induced by PM 2.5 were serious in the ACE2 KO mice compared with those in the WT mice. PM 2.5 treatment significantly increased pulmonary ACE expression and activity in both WT and ACE2 KO mice. Interestingly, pulmonary ACE2 activity in the WT mice was also induced. We hypothesized that increased ACE2 activity in the WT mice is a physiological response for increased ACE activity due to PM 2.5 exposure. However, the response is lack in the ACE2 KO mice because the mice being ACE2 deficiency. It is one of the reasons that serious physiopathology and inflammation induced by PM 2.5 in the ACE2 KO mice compared with those in the WT mice. Our data reveals that acute inflammation and lung injury could be induced by PM 2.5 treatment. The disorder of pulmonary RAS may aggravate the disease progressive of pulmonary system due to PM 2.5 exposure. Therefore, we propose that it may be helpful for the cardiopulmonary patients by RAS regulation when the patients are exposed to severe particulate pollutants.