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Measuring Carbon Content in Airway Macrophages Exposed to Carbon-Containing Particulate Matters
Published on: July 12, 2024
Urban particulate matter (PM) suppresses airway antibacterial defence
Xiaoyan Chen1, Jinguo Liu1, Jian Zhou1
1Department of Pulmonary Medicine, Zhongshan Hospital, Fudan University and Shanghai Respiratory Research Institute, 180 Fenglin Road, Shanghai, 200032, People's Republic of China.
Background:
Epidemiological studies have shown that urban particulate matter (PM) increases the risk of respiratory infection. However, the underlying mechanisms are poorly understood. PM has been postulated to suppress the activation of airway epithelial innate defence in response to infection.
Methods:
The effects of PM on antibacterial defence were studied using an in vitro infection model. The levels of antimicrobial peptides were measured using RT-PCR and ELISA. In addition to performing colony-forming unit counts and flow cytometry, confocal microscopy was performed to directly observe bacterial invasion upon PM exposure.
Results:
We found that PM PM increased bacterial invasion by impairing the induction of β-defensin-2 (hBD-2), but not the other antimicrobial peptides (APMs) secreted by airway epithelium. PM further increases bacteria-induced ROS production, which is accompanied by an accelerated cell senescence and a decrease in bacteria-induced hBD-2 production, and the antioxidant NAC treatment attenuates these effects. The PM exposure further upregulated the expression of IL-8 but downregulated the expression of IL-13 upon infection.
Conclusions:
PM promotes bacterial invasion of airway epithelial cells by attenuating the induction of hBD-2 via an oxidative burst. These findings associate PM with an increased susceptibility to infection. These findings provide insight into the underlying mechanisms regarding the pathogenesis of particulate matter.
Insights
Urban particulate matter (PM) increases respiratory infection risk by impairing airway epithelial defenses. PM exposure hinders beta-defensin-2 production, promoting bacterial invasion and increasing susceptibility to infections.
Area of Science:
- Environmental Health
- Infectious Disease Immunology
- Cell Biology
Background:
- Urban particulate matter (PM) is linked to increased respiratory infection risk.
- Mechanisms by which PM affects respiratory infections are not fully understood.
- PM may suppress airway epithelial innate immune responses to pathogens.
Purpose of the Study:
- To investigate the impact of PM on antibacterial defense mechanisms in airway epithelial cells.
- To elucidate the cellular and molecular pathways involved in PM-induced susceptibility to respiratory infections.
Main Methods:
- Utilized an in vitro infection model to study PM effects on airway epithelium.
- Quantified antimicrobial peptide levels using RT-PCR and ELISA.
- Assessed bacterial invasion via colony-forming unit counts, flow cytometry, and confocal microscopy.
Main Results:
- PM exposure increased bacterial invasion by impairing the induction of human beta-defensin-2 (hBD-2).
- PM enhanced reactive oxygen species (ROS) production, leading to accelerated cell senescence and reduced hBD-2 induction.
- Antioxidant N-acetylcysteine (NAC) treatment mitigated PM-induced effects; PM altered IL-8 and IL-13 expression.
Conclusions:
- PM promotes bacterial invasion by attenuating hBD-2 induction through an oxidative burst mechanism.
- These findings link PM exposure to increased susceptibility to respiratory infections.
- The study provides insights into the pathogenesis of particulate matter-related respiratory diseases.
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