Exposure to ambient particulate matter alters the microbial composition and induces immune changes in rat lung

Li, Naijian; He, Fang; Liao, Baoling; Yang, Zhou; Li, Bing; Ran, Pixin

doi:10.1186/s12931-017-0626-6

Cited by 53 publications

(36 citation statements)

References 43 publications

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“…In rats, exposure to biomass smoke has been shown to increase bacterial abundance and diversity in lung tissue, and particulate matter exposure significantly increased the capacity of alveolar macrophages to phagocytose bacteria (Li et al, ). Recently, a cross‐sectional study of bronchoalveolar lavage samples from 44 healthy adults in Malawi evaluated that association between HAP and the lung microbiome (Rylance et al, ).…”

Section: Discussionmentioning

confidence: 99%

The respiratory tract microbiome and its relationship to lung cancer and environmental exposures found in rural china

Hosgood

Mongodin

Wan

et al. 2019

Environ and Mol Mutagen

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We previously reported that bacterial diversity in sputum samples from never‐smoking women in rural China varied by lung cancer status and household air pollution (HAP) exposure type. Here, we expand on our associations between environmental exposures and respiratory tract microbiota with an additional 90 never‐smoking women from Xuanwei, China. DNA from sputum samples of cases (n = 45) and controls (n = 45) was extracted using a multistep enzymatic and physical lysis, followed by a standardized clean up. V1–V2 regions of 16S rRNA genes were Polymerase chain reaction (PCR) amplified. Purified amplicons were sequenced by 454 FLX Titanium pyrosequencing and high‐quality sequences were evaluated for diversity and taxonomic membership. In our population of never‐smokers, increased risk of lung cancer was associated with lower alpha diversity compared to higher alpha diversity (Shannon: ORhigh = 1.00 [reference], ORmedium = 3.84 [1.02–14.48], ORlow = 3.78 [1.03–13.82]; observed species: ORhigh = 1.00 [reference], ORmedium = 2.37 [0.67–8.48], ORlow = 2.01 [0.58–6.97]; Phylogenetic Diversity (PD) whole tree: ORhigh = 1.00 [reference], ORmedium = 3.04 [0.85–10.92], ORlow = 2.53 [0.72–8.96]), as well as a decreased relative abundance of Fusobacteria (ORhigh = 1.00 [reference], ORmedium = 1.24 [0.42–3.66], ORlow = 2.01 [0.63–6.44], ptrend = 0.03). Increasing alpha diversity was associated with smoky coal use compared to clean fuel use among all subjects (observed species, P = 0.001; PD whole tree, P = 0.006; Shannon, P = 0.0002), as well as cases (observed species, P = 0.02; PD whole tree, P = 0.03; Shannon, P = 0.03) and controls (observed species, P = 0.01; PD whole tree, P = 0.05; Shannon, P = 0.002). Increased diversity was also associated with presence of livestock (observed species, P = 0.02; PD whole tree, P = 0.02; Shannon, P = 0.03) in the home for cases. Our study is the first to report that decreased microbial diversity is associated with risk of lung cancer. Larger studies are necessary to elucidate the direct and indirect effects attributed to the disease‐specific, HAP‐specific, and animal‐specific associations. Environ. Mol. Mutagen. 2019. © 2019 Wiley Periodicals, Inc.

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Section: Discussionmentioning

confidence: 99%

The respiratory tract microbiome and its relationship to lung cancer and environmental exposures found in rural china

Hosgood

Mongodin

Wan

et al. 2019

Environ and Mol Mutagen

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“…The adverse health effects of inhaling PM have been widely studied in respiratory diseases, cardiovascular disease, and premature death (37)(38)(39), and the adverse respiratory health effects have drawn considerable worldwide attention over recent decades (5,(40)(41)(42)(43). Because particle sizes decide where the particle lands in the airway, much of the enthusiasm and effort has been drawn to PM 2.5 or even PM 0.1 (6).…”

Section: Discussionmentioning

confidence: 99%

MTOR Suppresses Environmental Particle-Induced Inflammatory Response in Macrophages

Chen

et al. 2018

The Journal of Immunology

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Increasing toxicological and epidemiological studies have demonstrated that ambient particulate matter (PM) could cause adverse health effects including inflammation in the lung. Alveolar macrophages represent a major type of innate immune responses to foreign substances. However, the detailed mechanisms of inflammatory responses induced by PM exposure in macrophages are still unclear. We observed that coarse PM treatment rapidly activated mechanistic target of rapamycin (MTOR) in mouse alveolar macrophages in vivo, and in cultured mouse bone marrow-derived macrophages, mouse peritoneal macrophages, and RAW264.7 cells. Pharmacological inhibition or genetic knockdown of MTOR in bone marrow-derived macrophages leads to an amplified cytokine production upon PM exposure, and mice with specific knockdown of MTOR or ras homolog enriched in brain in myeloid cells exhibit significantly aggregated airway inflammation. Mechanistically, PM activated MTOR through modulation of ERK, AKT serine/threonine kinase 1, and tuberous sclerosis complex signals, whereas MTOR deficiency further enhanced the PM-induced necroptosis and activation of subsequent NF κ light-chain-enhancer of activated B cells (NFKB) signaling. Inhibition of necroptosis or NFKB pathways significantly ameliorated PM-induced inflammatory response in MTOR-deficient macrophages. The present study thus demonstrates that MTOR serves as an early adaptive signal that suppresses the PM-induced necroptosis, NFKB activation, and inflammatory response in lung macrophages, and suggests that activation of MTOR or inhibition of necroptosis in macrophages may represent novel therapeutic strategies for PM-related airway disorders.

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“…They also allow for assessing more chronic exposure; while selective breeding and the availability of gene knockout strains allow the development of models of inheritable risks. Models have varied regarding the species used (for example rabbits [ 56 ], mice [ 57 , 58 , 59 ], rats [ 60 , 61 , 62 ], guinea pigs [ 63 , 64 ] as well as larger species such as dogs and sheep [ 65 , 66 ]), the nature of the exposure system (smoke from biomass, exposure to PM), and the length of the exposure (acute or chronic). In reporting on the findings of The Toxicology and Animal Study Design Workgroup at the 2009 International Biomass Smoke Health Effects (IBSHE) conference, Migliaccio and Mauderly stated that after reviewing many studies, it was only studies modeling COPD, emphysema, and the potential CNS effects that the working group were not confident about with regard to providing reliable data demonstrating the adverse effects of biomass smoke exposure [ 67 ].…”

Section: How Does Biomass Smoke Exposure Contribute To the Developmentioning

confidence: 99%

Evidence of Biomass Smoke Exposure as a Causative Factor for the Development of COPD

Capistrano

Reyk

Chen

et al. 2017

Toxics

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Chronic obstructive pulmonary disease (COPD) is a progressive disease of the lungs characterised by chronic inflammation, obstruction of airways, and destruction of the parenchyma (emphysema). These changes gradually impair lung function and prevent normal breathing. In 2002, COPD was the fifth leading cause of death, and is estimated by the World Health Organisation (WHO) to become the third by 2020. Cigarette smokers are thought to be the most at risk of developing COPD. However, recent studies have shown that people with life-long exposure to biomass smoke are also at high risk of developing COPD. Most common in developing countries, biomass fuels such as wood and coal are used for cooking and heating indoors on a daily basis. Women and children have the highest amounts of exposures and are therefore more likely to develop the disease. Despite epidemiological studies providing evidence of the causative relationship between biomass smoke and COPD, there are still limited mechanistic studies on how biomass smoke causes, and contributes to the progression of COPD. This review will focus upon why biomass fuels are used, and their relationship to COPD. It will also suggest methodological approaches to model biomass exposure in vitro and in vivo.

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Exposure to ambient particulate matter alters the microbial composition and induces immune changes in rat lung

Cited by 53 publications

References 43 publications

The respiratory tract microbiome and its relationship to lung cancer and environmental exposures found in rural china

The respiratory tract microbiome and its relationship to lung cancer and environmental exposures found in rural china

MTOR Suppresses Environmental Particle-Induced Inflammatory Response in Macrophages

Evidence of Biomass Smoke Exposure as a Causative Factor for the Development of COPD

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