scholarly journals Chronic exposure to ambient particulate matter induces gut microbial dysbiosis in a rat COPD model

2020 ◽  
Vol 21 (1) ◽  
Author(s):  
Naijian Li ◽  
Zhaowei Yang ◽  
Baoling Liao ◽  
Tianhui Pan ◽  
Jinding Pu ◽  
...  

Abstract Background The role of the microbiota in the pathogenesis of chronic obstructive pulmonary disease (COPD) following exposure to ambient particulate matter (PM) is largely unknown. Methods Fifty-four male Sprague-Dawley rats were exposed to clean air, biomass fuel (BMF), or motor vehicle exhaust (MVE) for 4, 12, and 24 weeks. We performed pulmonary inflammation evaluation, morphometric measurements, and lung function analysis in rat lung at three different times points during exposure. Lung and gut microbial composition was assessed by 16S rRNA pyrosequencing. Serum lipopolysaccharide levels were measured and short-chain fatty acids in colon contents were quantified. Results After a 24-week PM exposure, rats exhibited pulmonary inflammation and pathological changes characteristic of COPD. The control and PM exposure (BMF and MVE) groups showed similar microbial diversity and composition in rat lung. However, the gut microbiota after 24 weeks PM exposure was characterized by decreased microbial richness and diversity, distinct overall microbial composition, lower levels of short-chain fatty acids, and higher serum lipopolysaccharide. Conclusion Chronic exposure to ambient particulate matter induces gut microbial dysbiosis and metabolite shifts in a rat model of chronic obstructive pulmonary disease.

2020 ◽  
Author(s):  
Naijian Li ◽  
Zhaowei Yang ◽  
Baoling Liao ◽  
Tianhui Pan ◽  
Jinding Pu ◽  
...  

Abstract Background: The role of the microbiota in the pathogenesis of chronic obstructive pulmonary disease (COPD) following exposure to ambient particulate matter (PM) is largely unknown.Methods: Fifty-four male Sprague-Dawley rats were exposed to clean air, biomass fuel (BMF), or motor vehicle exhaust (MVE) for 4, 12, and 24 weeks. We performed pulmonary inflammation evaluation, morphometric measurements, and lung function analysis in rat lung at three different times points during exposure. Lung and gut microbial composition was assessed by 16S rRNA pyrosequencing. Serum lipopolysaccharide levels were measured and short-chain fatty acids in colon contents were quantified.Results: After a 24-week PM exposure, rats exhibited pulmonary inflammation and pathological changes characteristic of COPD. The control and PM exposure (BMF and MVE) groups showed similar microbial diversity and composition in rat lung. However, the gut microbiota after 24 weeks PM exposure was characterized by decreased microbial richness and diversity, distinct overall microbial composition, lower levels of short-chain fatty acids, and higher serum lipopolysaccharide.Conclusion: Chronic exposure to ambient particulate matter induces gut microbial dysbiosis and metabolite shifts in a rat model of chronic obstructive pulmonary disease.


2020 ◽  
Author(s):  
Naijian Li ◽  
Zhaowei Yang ◽  
Baoling Liao ◽  
Tianhui Pan ◽  
Jinding Pu ◽  
...  

Abstract Background: The role of the gut microbiota in the pathogenesis of chronic obstructive pulmonary disease following exposure to ambient particulate matter is largely unknown. We hypothesized that exposure alters gut microbial composition and metabolites and may involved in the pathogenesis of chronic obstructive pulmonary disease.Methods: Fifty-four male Sprague-Dawley rats were exposed to clean air, biomass fuel, or motor vehicle exhaust for 4, 12, and 24 weeks. Lung tissue was assessed histologically and gut microbial composition was assessed by 16S rRNA pyrosequencing. Serum lipopolysaccharide levels were measured and short-chain fatty acids in colon contents were quantified. Results: After a 24-week exposure to particulate matter, rats exhibited pulmonary inflammation and pathological changes characteristic of chronic obstructive pulmonary disease. The gut microbiome was characterized by decreased microbial richness and diversity, distinct overall microbial composition, lower levels of short-chain fatty acids, and higher serum lipopolysaccharide. Conclusion: Chronic exposure to ambient particulate matter induces gut microbial dysbiosis and metabolite shifts in a rat model of chronic obstructive pulmonary disease.


2020 ◽  
Author(s):  
Naijian Li ◽  
Zhaowei Yang ◽  
Baoling Liao ◽  
Tianhui Pan ◽  
Jinding Pu ◽  
...  

Abstract Background The role of the gut microbiota in the pathogenesis of chronic obstructive pulmonary disease following exposure to ambient particulate matter is largely unknown. We hypothesized that exposure alters gut microbial composition and metabolites and is involved in the pathogenesis of chronic obstructive pulmonary disease. Methods Fifty-four male Sprague-Dawley rats were exposed to clean air, biomass fuel, or motor vehicle exhaust for 4, 12, and 24 weeks. Lung tissue was assessed histologically and gut microbial composition was assessed by 16S rRNA pyrosequencing. Serum lipopolysaccharide levels were measured and short-chain fatty acids in colon contents were quantified. Results After a 24-week exposure to particulate matter, rats exhibited pulmonary inflammation and pathological changes characteristic of chronic obstructive pulmonary disease. The gut microbiome was characterized by decreased microbial richness and diversity, distinct overall microbial composition, lower levels of short-chain fatty acids, and higher serum lipopolysaccharide. Conclusion Chronic exposure to ambient particulate matter induces gut microbial dysbiosis and metabolite shifts in a rat model of chronic obstructive pulmonary disease.


2019 ◽  
Vol 317 (3) ◽  
pp. L424-L430 ◽  
Author(s):  
Yik Lung Chan ◽  
Baoming Wang ◽  
Hui Chen ◽  
Kin Fai Ho ◽  
Junji Cao ◽  
...  

Air pollution is a ubiquitous problem and comprises gaseous and particulate matter (PM). Epidemiological studies have clearly shown that exposure to PM is associated with impaired lung function and the development of lung diseases, such as chronic obstructive pulmonary disease and asthma. To understand the mechanisms involved, animal models are often used. However, the majority of such models represent high levels of exposure and are not representative of the exposure levels in less polluted countries, such as Australia. Therefore, in this study, we aimed to determine whether low dose PM10 exposure has any detrimental effect on the lungs. Mice were intranasally exposed to saline or traffic-related PM10 (1μg or 5μg/day) for 3 wk. Bronchoalveolar lavage (BAL) and lung tissue were analyzed. PM10 at 1 μg did not significantly affect inflammatory and mitochondrial markers. At 5 μg, PM10 exposure increased lymphocytes and macrophages in BAL fluid. Increased NACHT, LRR and PYD domains-containing protein 3 (NLRP3) and IL-1β production occurred following PM10 exposure. PM10 (5 μg) exposure reduced mitochondrial antioxidant manganese superoxide (antioxidant defense system) and mitochondrial fusion marker (OPA-1), while it increased fission marker (Drp-1). Autophagy marker light-chain 3 microtubule-associated protein (LC3)-II and phosphorylated-AMPK were reduced, and apoptosis marker (caspase 3) was increased. No significant change of remodeling markers was observed. In conclusion, a subchronic low-level exposure to PM can have an adverse effect on lung health, which should be taken into consideration for the planning of roads and residential buildings.


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