Mechanistic Insights into the Impact of Air Pollution on Pneumococcal Pathogenesis and Transmission

Beentjes, Daan; Shears, Rebecca K.; French, Neil; Neill, Daniel R.; Kadioglu, Aras

doi:10.1164/rccm.202112-2668tr

Cited by 15 publications

(9 citation statements)

References 167 publications

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“…Our collective findings were in line with existing mechanistic evidence that carbon particles can be capable of impairment in pulmonary host defense through several pathways, consequently heightened respiratory infections following air pollution exposure (Beentjes et al., 2022 ). Studies have revealed that carbon particles as biologically active stimuli can swiftly elicit pulmonary and systemic inflammatory responses (De Prins et al., 2014 ).…”

Section: Discussionsupporting

confidence: 91%

“…Emerging experimental evidence supports that air population exposure can prompt host defense abnormalities, thereby might play an important role in colonization and transmission of bacterial or viral infections in the airways (Beentjes et al., 2022 ). Mechanistically, inhalation of carbon particles is capable of exhibiting potent abilities to worsen airway functions, including reduced ciliary beat frequency, inhibited bioactivity of antimicrobial peptides, and enhanced mucus production (Beentjes et al., 2022 ). Further, exposure to particles has been shown to suppress capacity of immune cells (e.g., alveolar macrophages) to internalize pathogens and increase pneumococcal colonization in the lungs (Yin et al., 2007 ; Zhou & Kobzik, 2007 ).…”

Section: Introductionmentioning

confidence: 99%

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Ambient Anthropogenic Carbons and Pediatric Respiratory Infections: A Case‐Crossover Analysis in the Megacity Beijing

Song

et al. 2023

GeoHealth

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Carbon loading in airway cells has shown to worsen function of antimicrobial peptides, permitting increased survival of pathogens in the respiratory tract; however, data on the impacts of carbon particles on childhood acute respiratory infection (ARI) is limited. We assembled daily health data on outpatient visits for ARI (bronchitis, pneumonia, and total upper respiratory infection [TURI]) in children aged 0–14 years between 2015 and 2019 in Beijing, China. Anthropogenic carbons, including black carbon (BC) and its emission sources, and wood smoke particles (delta carbon, ultra‐violet absorbing particulate matter, and brown carbon) were continuously monitored. Using a time‐stratified case‐crossover approach, conditional logistic regression was performed to derive risk estimates for each outcome. A total of 856,899 children were included, and a wide range of daily carbon particle concentrations was observed, with large variations for BC (0.36–20.44) and delta carbon (0.48–57.66 μg/m3). Exposure to these particles were independently associated with ARI, with nearly linear exposure‐response relationships. Interquartile range increases in concentrations of BC and delta carbon over prior 0–8 days, we observed elevation of the odd ratio of bronchitis by 1.201 (95% confidence interval, 1.180, 1.221) and 1.048 (95% CI, 1.039, 1.057), respectively. Stronger association was observed for BC from traffic sources, which increased the odd ratio of bronchitis by 1.298 (95% CI, 1.273, 1.324). Carbon particles were also associated with elevated risks of pneumonia and TURI, and subgroup analyses indicated greater risks among children older than 6 years. Our findings suggested that anthropogenic carbons in metropolitan areas may pose a significant threat to clinical manifestations of respiratory infections in vulnerable populations.

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Section: Discussionsupporting

confidence: 91%

Section: Introductionmentioning

confidence: 99%

Ambient Anthropogenic Carbons and Pediatric Respiratory Infections: A Case‐Crossover Analysis in the Megacity Beijing

Song

et al. 2023

GeoHealth

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“…This study found that air pollution had a positive association with the burden of meningitis, which may be related to multiple mechanisms. Air pollution particles may make pathogen colonization possible by reducing mucosal ciliary clearance, reducing the barrier effect of the airways, and dysregulating the airway microbiota, while air pollution may enhance the inflammatory response of the body and enhance the transmission of pathogens such as S. pneumoniae to tissues and blood, causing carriers to be more likely to develop meningitis and resulting in higher ASDRs and ASYRs [ 34 , 35 ]. Before our study, a large body of current research focused on the association between meningitis incidence and dust/pm2.5, and most of the studies were limited to a single country [ 36 , 37 ].…”

Section: Discussionmentioning

confidence: 99%

Global Burden and Its Association with Socioeconomic Development Status of Meningitis Caused by Specific Pathogens over the Past 30 years: A Population-Based Study

Cheng¹,

Qu²,

Wang³

et al. 2023

Neuroepidemiology

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Background: Meningitis is a severe and fatal neurological disease and causes lots of disease burden. The purpose of this study was to assess the global, regional, and national burdens and trends of meningitis by age, sex, and etiology. Methods: Data on the burden of meningitis were collected from the Global Burden of Diseases, Injuries, and Risk Factors Study 2019. R and Joinpoint were used for statistical analysis and charting. Results: In 2019, meningitis caused 236,222 deaths and 15,649,865 years of life lost (YLL) worldwide. The age-standardized death rate and age-standardized YLL rate of meningitis were 3.29 and 225, which decreased steadily. Burden change was mainly driven by epidemiological changes. Regionally, meningitis burden was the highest in Sub-Saharan Africa. Burden of disease increasingly concentrated in low sociodemographic index countries, and this was most pronounced in meningitis caused by N. meningitidis. Countries such as Mali, Nigeria, Sierra Leone, etc., especially need to enhance the rational allocation of public health resources to reduce the disease burden. Children and men were more likely to be affected by meningitis. PM2.5 was found to be an important risk factor. Conclusions: This study provides the first comprehensive understanding of the global disease burden of meningitis caused by specific pathogens and highlights policy priorities to protect human health worldwide, with particular attention to vulnerable regions, susceptible populations, environmental factors, and specific pathogens.

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“…Similarly, we found that the macrophages in the BALF tended to be elevated without statistical significance in the mice after 3-month DEE exposure. More importantly, it has been shown that the phagocytic rate and phagocytic index of macrophages are significantly reduced after exposure to certain particulate matter, suggesting inhibited phagocytic activity [ 8 , 9 , 10 , 11 , 32 ]. However, DEP can form aggregates of different sizes and subsequently impair the phagocytic ability of alveolar macrophages, resulting in deleterious health effects [ 33 ].…”

Section: Discussionmentioning

confidence: 99%

CXCL17 Attenuates Diesel Exhaust Emissions Exposure-Induced Lung Damage by Regulating Macrophage Function

Yin

Wang

et al. 2023

Toxics

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Exposure to diesel exhaust emissions (DEE) is strongly linked to innate immune injury and lung injury, but the role of macrophage chemoattractant CXCL17 in the lung damage caused by DEE exposure remains unclear. In this study, whole-body plethysmography (WBP), inflammatory cell differential count, and histopathological analysis were performed to assess respiratory parameters, airway inflammation, and airway injury in C57BL/6 male mice exposed to DEE for 3 months. qRT-PCR, IHC (immunohistochemistry), and ELISA were performed to measure the CXCL17 expression in airway epithelium or BALF (bronchoalveolar lavage fluid) following DEE/Diesel exhaust particle (DEP) exposure. Respiratory parameters, airway inflammation, and airway injury were assessed in CXCL17-overexpressing mice through adeno-associated virus vector Type 5 (AAV5) infection. Additionally, an in vitro THP-1 and HBE co-culture system was constructed. Transwell assay was carried out to evaluate the effect of rh-CXCL17 (recombinant human protein-CXCL17) on THP-1 cell migration. Flow cytometry and qRT-PCR were conducted to assess the impacts of rh-CXCL17 on apoptosis and inflammation/remodeling of HBE cells. We found that the mice exposed to DEE showed abnormal respiratory parameters, accompanied by airway injury and remodeling (ciliary injury in airway epithelium, airway smooth muscle hyperplasia, and increased collagen deposition). Carbon content in airway macrophages (CCAM), but not the number of macrophages in BALF, increased significantly. CXCL17 expression significantly decreased in mice airways and HBE after DEE/DEP exposure. AAV5-CXCL17 enhanced macrophage recruitment and clearance of DEE in the lungs of mice, and it improved respiratory parameters, airway injury, and airway remodeling. In the THP-1/HBE co-culture system, rh-CXCL17 increased THP-1 cell migration while attenuating HBE cell apoptosis and inflammation/remodeling. Therefore, CXCL17 might attenuate DEE-induced lung damage by recruiting and activating pulmonary macrophages, which is expected to be a novel therapeutic target for DEE-associated lung diseases.

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Mechanistic Insights into the Impact of Air Pollution on Pneumococcal Pathogenesis and Transmission

Cited by 15 publications

References 167 publications

Ambient Anthropogenic Carbons and Pediatric Respiratory Infections: A Case‐Crossover Analysis in the Megacity Beijing

Ambient Anthropogenic Carbons and Pediatric Respiratory Infections: A Case‐Crossover Analysis in the Megacity Beijing

Global Burden and Its Association with Socioeconomic Development Status of Meningitis Caused by Specific Pathogens over the Past 30 years: A Population-Based Study

CXCL17 Attenuates Diesel Exhaust Emissions Exposure-Induced Lung Damage by Regulating Macrophage Function

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