Dataset Information

PM_2.5 impairs macrophage functions to exacerbate pneumococcus-induced pulmonary pathogenesis.

ABSTRACT:

Background

Pneumococcus is one of the most common human airway pathogens that causes life-threatening infections. Ambient fine particulate matter (PM) with aerodynamic diameter ≤ 2.5 μm (PM_2.5) is known to significantly contribute to respiratory diseases. PM_2.5-induced airway inflammation may decrease innate immune defenses against bacterial infection. However, there is currently limited information available regarding the effect of PM_2.5 exposure on molecular interactions between pneumococcus and macrophages.

Results

PM_2.5 exposure hampered macrophage functions, including phagocytosis and proinflammatory cytokine production, in response to pneumococcal infection. In a PM_2.5-exposed pneumococcus-infected mouse model, PM_2.5 subverted the pulmonary immune response and caused leukocyte infiltration. Further, PM_2.5 exposure suppressed the levels of CXCL10 and its receptor, CXCR3, by inhibiting the PI3K/Akt and MAPK pathways.

Conclusions

The effect of PM_2.5 exposure on macrophage activity enhances pneumococcal infectivity and aggravates pulmonary pathogenesis.

SUBMITTER: Chen YW

PROVIDER: S-EPMC7409448 | biostudies-literature | 2020 Aug

REPOSITORIES: biostudies-literature

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Publications

PM<sub>2.5</sub> impairs macrophage functions to exacerbate pneumococcus-induced pulmonary pathogenesis.

Chen Yu-Wen YW Huang Mei-Zi MZ Chen Chyi-Liang CL Kuo Chieh-Ying CY Yang Chia-Yu CY Chiang-Ni Chuan C Chen Yi-Ywan M YM Hsieh Chia-Ming CM Wu Hui-Yu HY Kuo Ming-Ling ML Chiu Cheng-Hsun CH Lai Chih-Ho CH

Particle and fibre toxicology 20200804 1

<h4>Background</h4>Pneumococcus is one of the most common human airway pathogens that causes life-threatening infections. Ambient fine particulate matter (PM) with aerodynamic diameter ≤ 2.5 μm (PM<sub>2.5</sub>) is known to significantly contribute to respiratory diseases. PM<sub>2.5</sub>-induced airway inflammation may decrease innate immune defenses against bacterial infection. However, there is currently limited information available regarding the effect of PM<sub>2.5</sub> exposure on mole ...[more]

PMID: 32753046

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Project description:BackgroundCigarette smoking and particulate matter (PM) with aerodynamic diameter < 2.5 μm (PM2.5) are major preventable cardiovascular mortality and morbidity promoters. Their joint role in metabolic syndrome (MS) pathogenesis is unknown. We determined the risk of MS based on PM2.5 and cigarette smoking in Taiwanese adults.MethodsThe study included 126,366 Taiwanese between 30 and 70 years old with no personal history of cancer. The Taiwan Biobank (TWB) contained information on MS, cigarette smoking, and covariates, while the Environmental Protection Administration (EPA), Taiwan, contained the PM2.5 information. Individuals were categorized as current, former, and nonsmokers. PM2.5 levels were categorized into quartiles: PM2.5 ≤ Q1, Q1 < PM2.5 ≤ Q2, Q2 < PM2.5 ≤ Q3, and PM2.5 > Q3, corresponding to PM2.5 ≤ 27.137, 27.137 < PM2.5 ≤ 32.589, 32.589 < PM2.5 ≤ 38.205, and PM2.5 > 38.205 μg/m3.ResultsThe prevalence of MS was significantly different according to PM2.5 exposure (p-value = 0.0280) and cigarette smoking (p-value < 0.0001). Higher PM2.5 levels were significantly associated with a higher risk of MS: odds ratio (OR); 95% confidence interval (CI) = 1.058; 1.014-1.104, 1.185; 1.134-1.238, and 1.149; 1.101-1.200 for 27.137 < PM2.5 ≤ 32.589, 32.589 < PM2.5 ≤ 38.205, and PM2.5 > 38.205 μg/m3, respectively. The risk of MS was significantly higher among former and current smokers with OR; 95% CI = 1.062; 1.008-1.118 and 1.531; 1.450-1.616, respectively, and a dose-dependent p-value < 0.0001. The interaction between both exposures regarding MS was significant (p-value = 0.0157). Stratification by cigarette smoking revealed a significant risk of MS due to PM2.5 exposure among nonsmokers: OR (95% CI) = 1.074 (1.022-1.128), 1.226 (1.166-1.290), and 1.187 (1.129-1.247) for 27.137 < PM2.5 ≤ 32.589, 32.589 < PM2.5 ≤ 38.205, and PM2.5 > 38.205 μg/m3, respectively. According to PM2.5 quartiles, current smokers had a higher risk of MS, regardless of PM2.5 levels (OR); 95% CI = 1.605; 1.444-1.785, 1.561; 1.409-1.728, 1.359; 1.211-1.524, and 1.585; 1.418-1.772 for PM2.5 ≤ 27.137, 27.137 < PM2.5 ≤ 32.589, 32.589 < PM2.5 ≤ 38.205, and PM2.5 > 38.205 μg/m3, respectively. After combining both exposures, the group, current smokers; PM2.5 > 38.205 μg/m3 had the highest odds (1.801; 95% CI =1.625-1.995).ConclusionPM2.5 and cigarette smoking were independently and jointly associated with a higher risk of MS. Stratified analyses revealed that cigarette smoking might have a much higher effect on MS than PM2.5. Nonetheless, exposure to both PM2.5 and cigarette smoking could compound the risk of MS.

Project description:BackgroundAir pollution is the greatest environmental threat to human health in the world today and is responsible for an estimated 7-9 million deaths annually. One of the most damaging air pollutants is PM2.5 pollution, fine airborne particulate matter under 2.5 microns in diameter. Exposure to PM2.5 pollution can cause premature death, heart disease, lung cancer, stroke, diabetes, asthma, low birthweight, and IQ loss. To avoid these adverse health effects, the WHO recommends that PM2.5 levels not exceed 5 μg/m3.MethodsThis study estimates the negative health impacts of PM2.5 pollution in Texas in 2016. Local exposure estimates were calculated at the census tract level using the EPA's BenMAP-CE software. In BenMAP, a variety of exposure-response functions combine air pollution exposure data with population data and county-level disease and death data to estimate the number of health effects attributable to PM2.5 pollution for each census tract. The health effects investigated were mortality, low birthweight, stroke, new onset asthma, new onset Alzheimer's, and non-fatal lung cancer.FindingsThis study found that approximately 26.7 million (98.9%) of the 27.0 million people living in Texas in 2016 resided in areas where PM2.5 concentrations were above the WHO recommendation of 5 μg/m3, and that 2.6 million people (9.8%) lived in areas where the average PM2.5 concentration exceeded 10 μg/m3. This study estimates that there were 8,405 (confidence interval [CI], 5,674-11,033) premature deaths due to PM2.5 pollution in Texas in 2016, comprising 4.3% of all deaths. Statewide increases in air-pollution-related morbidity and mortality were seen for stroke (2,209 - CI: [576, 3,776]), low birthweight (2,841 - CI: [1,696, 3,925]), non-fatal lung cancers (636 - CI: [219, 980]), new onset Alzheimer's disease (24,575 - CI: [20,800, 27,540]), and new onset asthma (7,823 - CI: [7,557, 8,079]).ConclusionThis study found that air pollution poses significant risks to the health of Texans, despite the fact that pollution levels across most of the state comply with the EPA standard for PM2.5 pollution of 12 μg/m3. Improving air quality in Texas could save thousands of lives from disease, disability, and premature death.

Project description:IntroductionDespite the London Underground (LU) handling on average 2.8 million passenger journeys per day, the characteristics and potential health effects of the elevated concentrations of metal-rich PM2.5 found in this subway system are not well understood.MethodsSpatial monitoring campaigns were carried out to characterise the health-relevant chemical and physical properties of PM2.5 across the LU network, including diurnal and day-to-day variability and spatial distribution (above ground, depth below ground and subway line). Population-weighted station PM2.5 rankings were produced to understand the relative importance of concentrations at different stations and on different lines.ResultsThe PM2.5 mass in the LU (mean 88 μg m-3, median 28 μg m-3) was greater than at ambient background locations (mean 19 μg m-3, median 14 μg m-3) and roadside environments in central London (mean 22 μg m-3, median 14 μg m-3). Concentrations varied between lines and locations, with the deepest and shallowest submerged lines being the District (median 4 μg m-3) and Victoria (median 361 μg m-3 but up to 885 μg m-3). Broadly in agreement with other subway systems around the world, sampled LU PM2.5 comprised 47% iron oxide, 7% elemental carbon, 11% organic carbon, and 14% metallic and mineral oxides. Although a relationship between line depth and air quality inside the tube trains was evident, there were clear influences relating to the distance from cleaner outside air and the exchange with cabin air when the doors open. The passenger population-weighted exposure analysis demonstrated a method to identify stations that should be prioritised for remediation to improve air quality.ConclusionPM2.5 concentrations in the LU are many times higher than in other London transport Environments. Failure to include this environment in epidemiological studies of the relationship between PM2.5 and health in London is therefore likely to lead to a large exposure misclassification error. Given the significant contribution of underground PM2.5 to daily exposure, and the differences in composition compared to urban PM2.5, there is a clear need for well-designed studies to better understand the health effects of underground exposure.

Dataset Information

PM_2.5 impairs macrophage functions to exacerbate pneumococcus-induced pulmonary pathogenesis.

Background

Results

Conclusions

Publications

PM<sub>2.5</sub> impairs macrophage functions to exacerbate pneumococcus-induced pulmonary pathogenesis.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets

Dataset Information

PM2.5 impairs macrophage functions to exacerbate pneumococcus-induced pulmonary pathogenesis.

Background

Results

Conclusions

Publications

PM<sub>2.5</sub> impairs macrophage functions to exacerbate pneumococcus-induced pulmonary pathogenesis.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets

PM_2.5 impairs macrophage functions to exacerbate pneumococcus-induced pulmonary pathogenesis.