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Obstructive Lung Diseases: COPD: Etiology |

PM2.5 and Cigarette Smoke Decrease Phagocytosis of Bacteria by Macrophages in Copd FREE TO VIEW

Xiaoju Liu, PhD; Xiaoli Zeng; Kai Shi; Qi Pang
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The First Hospital of Lanzhou University, Lanzhou, China


Copyright 2016, American College of Chest Physicians. All Rights Reserved.


Chest. 2016;149(4_S):A358. doi:10.1016/j.chest.2016.02.373
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SESSION TITLE: COPD: Etiology

SESSION TYPE: Original Investigation Poster

PRESENTED ON: Saturday, April 16, 2016 at 11:45 AM - 12:45 PM

PURPOSE: Epidemiological studies have shown that exposure to ambient fine particulate matter (PM2.5) and cigarette smoke links with an increased risk of respiratory deaths and hospital admission of chronic obstructive pulmonary disease (COPD). The reasons for this are unclear. In this study, we aimed to investigate the phagocytic capacity and oxidative damage of monocyte-derived macrophages (MDM) exposure to cigarette smoke extract (CSE) and PM2.5 in COPD.

METHODS: MDM were obtained from 32 COPD patients and 26 healthy subjects and exposed to PM2.5 collected from Lanzhou, China and CSE. Phagocytosis of fluorescein isothiocyanate (FITC) labelled Escherichia coli (FITC-E. coli) by MDM was assessed by flow cytometry and confocal microscopy. Moreover, PM2.5 and CSE-induced oxidative damage in MDM cells was observed through the alteration of malondialdehyde (MDA) content, total antioxidative capacity (TAC) and glutathione peroxidase (GSH-PX) activity in supernate.

RESULTS: PM2.5 or CSE treatment significantly decreased the phagocytic activity of MDM from COPD patients and healthy subjects. This inhibiting effect presented more obvious when the two combined. Additionally, the decrease of phagocytic activity was more in COPD MDM compared to healthy subjects. In COPD patients, the MDA content was higher than in healthy subjects, while the TAC level and GSH-PX activity were lower. PM2.5 or/and CSE decreased the MDA content and increased the the TAC level and GSH-PX activity in COPD patients and healthy subjects. This oxidative damage seen in COPD patients was more compared to healthy subjects. There was a negative correlation between the phagocytic activity and the levels of MDA exposured to in PM2.5 or/and CSE, whereas there is a positive correlation between the phagocytic activity and the levels of TAC and GSH-PX activities.

CONCLUSIONS: These results suggest that PM2.5 or/and CSE-induced oxidative stress, which may contribute to PM2.5 or/and CSE-induced impairment of phagocytic function of macrophage. COPD macrophage phagocytic responses are suppressed and may lead to bacterial colonization and increased exacerbation frequency.

CLINICAL IMPLICATIONS: PM2.5 or CSE impaired the phagocytic function of MDM, which could be the cause of increased susceptibility to infections in patients with COPD. PM2.5 or CSE induced oxidative stress probably plays a key role in phagocytosis in MDM. This provide a theoretical basis for the prevention and treatment of COPD.

DISCLOSURE: The following authors have nothing to disclose: Xiaoju Liu, Xiaoli Zeng, Kai Shi, Qi Pang

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