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

Li, Naijian; Yang, Zujun; Liao, Baoling; Pan, Tianhui; Pu, Jinding; Hao, Bin; Fu, Zhenli; Cao, Weitao; Yang, Zhou; He, Fang; Li, Bing; Ran, Pixin

doi:10.1186/s12931-020-01529-3

Cited by 26 publications

(17 citation statements)

References 32 publications

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“…In this study, the levels of SCFAs in stool from COPD III–IV patients were significantly lower than in stool from the other groups. This seems to be consistent with our previous research, that is gut microbial dysbiosis and lower levels of short-chain fatty acids were observed in a particulate matter-induced rat COPD model [ 27 ]. SCFAs have anti-inflammatory properties, improve gut barrier function and reduce intestinal bacterial translocation in the host.…”

Section: Discussionsupporting

confidence: 93%

“…Similar to the previous, a total of 60 mice were also randomly divided into four groups of 15: PBS FMT group, healthy FMT group, COPD I–II patients FMT group, and COPD III–IV patients FMT group. After microbiota depletion, all mice were exposed to smoke produced by smoldering China fir sawdust (40 g/exposure) for two 3-h periods, 5 days per week, for 20 weeks in an inhalation chamber (model INH-WB_NOE (R/M)_CAP (PM2.5)_CS_SP; TSE Systems, Bad Homburg, Germany) [ 27 ]. Particulate matter mass concentrations, particle size distributions, and gas concentrations (oxygen, carbon monoxide, nitrogen oxides, and sulfur dioxide) were monitored by a DustTrak II aerosol monitor 8530 (TSI, Shoreview, MN, USA) and a Testo 340 portable flue gas analyzer (Testo, Lenzkirch, Germany) in the exposure rooms.…”

Section: Animal Experimentsmentioning

confidence: 99%

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Gut microbiota dysbiosis contributes to the development of chronic obstructive pulmonary disease

Dai

Wang

et al. 2021

Respir Res

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Background Dysbiosis of the gut microbiome is involved in the pathogenesis of various diseases, but the contribution of gut microbes to the progression of chronic obstructive pulmonary disease (COPD) is still poorly understood. Methods We carried out 16S rRNA gene sequencing and short-chain fatty acid analyses in stool samples from a cohort of 73 healthy controls, 67 patients with COPD of GOLD stages I and II severity, and 32 patients with COPD of GOLD stages III and IV severity. Fecal microbiota from the three groups were then inoculated into recipient mice for a total of 14 times in 28 days to induce pulmonary changes. Furthermore, fecal microbiota from the three groups were inoculated into mice exposed to smoke from biomass fuel to induce COPD-like changes. Results We observed that the gut microbiome of COPD patients varied from that of healthy controls and was characterized by a distinct overall microbial diversity and composition, a Prevotella-dominated gut enterotype and lower levels of short-chain fatty acids. After 28 days of fecal transplantation from COPD patients, recipient mice exhibited elevated lung inflammation. Moreover, when mice were under both fecal transplantation and biomass fuel smoke exposure for a total of 20 weeks, accelerated declines in lung function, severe emphysematous changes, airway remodeling and mucus hypersecretion were observed. Conclusion These data demonstrate that altered gut microbiota in COPD patients is associated with disease progression in mice model.

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Section: Discussionsupporting

confidence: 93%

Section: Animal Experimentsmentioning

confidence: 99%

Gut microbiota dysbiosis contributes to the development of chronic obstructive pulmonary disease

Dai

Wang

et al. 2021

Respir Res

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“…However, this effect might be due to the slight increase of total iso-SCFAs, valeric acid, and iso-valeric acid levels induced by LPS treatment. Although we did not find a change in total SCFAs concentrations, in another COPD model, ambient particulate matter exposure induces gut microbial dysbiosis, and as a consequence, a decrease in total SCFA levels was observed ( 52 ). Cecal levels of valeric acid were also significantly decreased in cigarette smoke-exposed rats, which was associated with a decreased population of Bifidobacterium and an increase in cecum pH ( 53 ).…”

Section: Discussionmentioning

confidence: 56%

Changes in intestinal homeostasis and immunity in a cigarette smoke- and LPS-induced murine model for COPD: the lung-gut axis

Wang

Pelgrim

Marzal

et al. 2022

American Journal of Physiology-Lung Cellular and Molecular Phys

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Chronic obstructive pulmonary disease (COPD) is often associated with intestinal comorbidities. In this study, changes in intestinal homeostasis and immunity in a cigarette smoke and lipopolysaccharide (LPS)-induced COPD model were investigated. Mice were exposed to cigarette smoke or air for 72 days, except days 42, 52 and 62 on which the mice were treated with saline or LPS via intratracheal instillation. Cigarette smoke exposure increased the airway inflammatory cell numbers, mucus production and different inflammatory mediators, including C-reactive protein (CRP) and keratinocyte-derived chemokine (KC), in bronchoalveolar lavage (BAL) fluid and serum. LPS did not further impact airway inflammatory cell numbers or mucus production but decreased inflammatory mediators levels in BAL fluid. T helper (Th) 1 cells were enhanced in the spleen after cigarette smoke exposure, however, in combination with LPS caused an increase in Th1 and Th2 cells. Histomorphological changes were observed in the proximal small intestine after cigarette smoke exposure and addition of LPS had no effect. Cigarette smoke activated the intestinal immune network for IgA production in the distal small intestine which was associated with increased fecal sIgA levels and enlargement of Peyer's patches. Cigarette smoke plus LPS decreased fecal sIgA levels and the size of Peyer's patches. In conclusion, cigarette smoke with or without LPS affects intestinal health as observed by changes in intestinal histomorphology and immune network for IgA production. Elevated systemic mediators might play a role in the lung-gut crosstalk. These findings contribute to a better understanding of intestinal disorders related to COPD.

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“…Invasive lung function measurement was examined using a ventilated bias flow whole-body plethysmograph (WBP) (BioSystem XA, DSI, Wilmington, NC) under anaesthesia by Zoletil, which consisted of a reference chamber and animal chamber interconnected by a pressure transducer (MAX1320, Buxco Electronics, Sharon, CT). According to the Buxco pulmonary maneuvers protocol and previous reports [ 66 – 68 ], data for forced expiratory flow at 25–75% of forced vital capacity (FEF 25–75% ) and forced expiratory volume in 20 ms to forced vital capacity (FEV 20 /FVC) were presented. At least three acceptable maneuvers for each test of every rat were conducted to obtain a reliable mean spirometry data.…”

Section: Methodsmentioning

confidence: 99%

Prolonged exposure to traffic-related particulate matter and gaseous pollutants implicate distinct molecular mechanisms of lung injury in rats

et al. 2021

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Background Exposure to air pollution exerts direct effects on respiratory organs; however, molecular alterations underlying air pollution-induced pulmonary injury remain unclear. In this study, we investigated the effect of air pollution on the lung tissues of Sprague-Dawley rats with whole-body exposure to traffic-related PM1 (particulate matter < 1 μm in aerodynamic diameter) pollutants and compared it with that in rats exposed to high-efficiency particulate air–filtered gaseous pollutants and clean air controls for 3 and 6 months. Lung function and histological examinations were performed along with quantitative proteomics analysis and functional validation. Results Rats in the 6-month PM1-exposed group exhibited a significant decline in lung function, as determined by decreased FEF25–75% and FEV20/FVC; however, histological analysis revealed earlier lung damage, as evidenced by increased congestion and macrophage infiltration in 3-month PM1-exposed rat lungs. The lung tissue proteomics analysis identified 2673 proteins that highlighted the differential dysregulation of proteins involved in oxidative stress, cellular metabolism, calcium signalling, inflammatory responses, and actin dynamics under exposures to PM1 and gaseous pollutants. The presence of PM1 specifically enhanced oxidative stress and inflammatory reactions under subchronic exposure to traffic-related PM1 and suppressed glucose metabolism and actin cytoskeleton signalling. These factors might lead to repair failure and thus to lung function decline after chronic exposure to traffic-related PM1. A detailed pathogenic mechanism was proposed to depict temporal and dynamic molecular regulations associated with PM1- and gaseous pollutants-induced lung injury. Conclusion This study explored several potential molecular features associated with early lung damage in response to traffic-related air pollution, which might be used to screen individuals more susceptible to air pollution.

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

Cited by 26 publications

References 32 publications

Gut microbiota dysbiosis contributes to the development of chronic obstructive pulmonary disease

Gut microbiota dysbiosis contributes to the development of chronic obstructive pulmonary disease

Changes in intestinal homeostasis and immunity in a cigarette smoke- and LPS-induced murine model for COPD: the lung-gut axis

Prolonged exposure to traffic-related particulate matter and gaseous pollutants implicate distinct molecular mechanisms of lung injury in rats

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