Recently, many researchers paid more attentions to the association between air pollution and chronic obstructive pulmonary disease (COPD). Haze, a severe form of outdoor air pollution, affected most parts of northern and eastern China in the past winter. In China, studies have been performed to evaluate the impact of outdoor air pollution and biomass smoke exposure on COPD; and most studies have focused on the role of air pollution in acutely triggering symptoms and exacerbations. Few studies have examined the role of air pollution in inducing pathophysiological changes that characterise COPD. Evidence showed that outdoor air pollution affects lung function in both children and adults and triggers exacerbations of COPD symptoms. Hence outdoor air pollution may be considered a risk factor for COPD mortality. However, evidence to date has been suggestive (not conclusive) that chronic exposure to outdoor air pollution increases the prevalence and incidence of COPD. Cross-sectional studies showed biomass smoke exposure is a risk factor for COPD. A long-term retrospective study and a long-term prospective cohort study showed that biomass smoke exposure reductions were associated with a reduced decline in forced expiratory volume in 1 second (FEV1) and with a decreased risk of COPD. To fully understand the effect of air pollution on COPD, we recommend future studies with longer follow-up periods, more standardized definitions of COPD and more refined and source-specific exposure assessments.
ObjectiveTo establish a methodology for alveolar macrophages (AMs) phagocytosis of AlexaFluor 488 (AF488) labeled bacteria by flow cytometry.MethodsStaphylococcus aureus and Streptococcus pneumoniae were labeled with different concentrations of AF488. A flow cytometric assay was used to quantify in vivo bacterial uptake by AMs. AMs and different ratio of fluorescent-labeled bacteria were incubated at 37 ℃ for 2 hours, 4 hours, 6 hours and 8 hours, respectively. AMs were washed with DPBS and extracellular fluorescence was quenched with 1% (w/v) trypan blue. Trypan blue was aspirated and phagocytosis of fluorescent-labeled bacteria by AMs was measured using a flow cytometry. Confocal microscopy was performed to ensure that bacterial in positive AM had been internalized rather than bound to the cell surface.ResultsWhen the concentration of AF488 was more than 50 μg/mL, the labeling rates of Staphylococcus aureus and Streptococcus pneumoniae were higher than 92% (P<0.05), and has quickly reached the upper limit. With the prolongation of incubation time, the phagocytic rate of AMs increased from 20.4% at 2 hours to 76.5% at 8 hours. With the increase in the number of bacteria, the phagocytic rate of AMs increased from 7.7% by ratio of 1∶10 to 85.1% by ratio of 1∶300.ConclusionDetection of AMs phagocytosis of AF488 labeled bacteria by flow cytometry is an effective method, but the dye concentration, incubation time and the proportion of bacteria will influence the results.
ObjectiveTo establisht a gut microbiota mice model for chronic obstructive pulmonary disease (COPD) with fecal microbiota transplantation (FMT) and its evaluation.MethodsThe mice received FMT from healthy individuals, COPD Ⅰ-Ⅱ subjects, or COPD Ⅲ–Ⅳ subjects. After microbiota depletion, the FMT was performed by a single oral administration of 100 μL per mouse every other day, for a total of 14 times in 28 days. On the 29th day, the peripheral blood mononuclear cells were analyzed, the gut microbiota of mice before and after FMT was analyzed by 16S rRNA sequencing, and the mice model were evaluated.ResultsThe operational taxonomic units, Chao 1 and Shannon indexes of mice all decreased significantly after antibiotic treatment (P<0.001), but increased significantly after FMT from healthy individuals, COPD Ⅰ-Ⅱ subjects, or COPD Ⅲ–Ⅳ subjects (P<0.05 or P<0.01). The abundance of Firmicutes, Proteobacteria and Actinobacteria in the guts of the mice in the healthy human FMT group, COPD Ⅰ-Ⅱ FMT group and COPD Ⅲ-Ⅳ FMT group were significantly different from those of the control group who only received phosphate buffer saline instead of FMT (P<0.05 or P<0.01). The auxiliary T lymphocytes and cytotoxic T lymphocytes were higher, but B lymphocytes decreased in the peripheral blood of the mice in the COPD Ⅰ-Ⅱ FMT group and COPD Ⅲ-Ⅳ FMT group (P<0.05 or P<0.01).ConclusionFMT can successfully establish a COPD gut microbiota research model.
【Abstract】Objective To investigate the contribution of occupational exposure to dusts / gases / fumes to chronic obstructive pulmonary disease( COPD) and respiratory symptoms in China. Methods Based on the crosssectional survey of COPD which was conducted in urban and rural areas of Beijing, Shanghai, Guangdong,Liaoning, Tianjin, Chongqing and Shanxi for residents aged 40 years or older, the association between the occupational exposure to dusts/ gases/ fumes and COPD and respiratory symptoms was analyzed. The recruited populations were interviewed with questionnaire and were tested with spirometry. The post-bronchodilators FEV1 /FVC lt; 70% was used as diagnostic criteria of COPD. Having any cough, sputum, wheezing and dyspnea was defined as having respiratory symptoms. Results The prevalence of occupational exposure to dusts/ gases /fumes was 20. 5% . As shown by multiple-variables Logistic regression analyses, occupational exposure to dusts / fumes /gases [ OR = 1. 20 ( 1. 04, 1. 39) ] and dusts of grain [ 1. 48 ( 1. 18, 1. 86) ] were associated with COPD;occupational exposure to dusts / fumes / gases [ OR = 1. 37( 1. 25, 1. 49) ] , hard-rock mining [ OR = 2. 31( 1. 67,3. 20) ] , coal mining [ OR = 1. 71( 1. 09, 2. 70) ] , dusts of cement [ OR = 1. 92( 1. 47, 2. 52) ] , chemical or plastics manufacturing [ OR =1. 58( 1. 37, 1. 83) ] , spray painting [ OR= 1. 46( 1. 16, 1. 84) ] , and other dusts or fumes [ OR = 1. 46 ( 1. 29, 1. 64 ) ] were associated with the respiratory symptoms. Smoking and occupational exposure to dusts / gases / fumes had synergic effects on the increasing risk of respiratory symptoms. The populationattributable risk ( PAR) of exposure to dusts / gases / fumes was 3. 94% and 7. 05% for COPD and respiratory symptoms respectively. Conclusions Occupational exposure to dusts /gases /fumes is associated with COPD and respiratory symptoms. Smoking and occupational exposure to dusts/ gases /fumes may have synergic effects on respiratory symptoms.