Fine particulate matter manipulates immune response to exacerbate microbial pathogenesis in the respiratory tract

Abstract

Particulate matter with a diameter ≤2.5 μm (PM_2.5) poses a substantial global challenge, with a growing recognition of pathogens contributing to diseases associated with exposure to PM_2.5 Recent studies have focused on PM_2.5, which impairs the immune cells in response to microbial infections and potentially contributes to the development of severe diseases in the respiratory tract. Accordingly, changes in the respiratory immune function and microecology mediated by PM_2.5 are important factors that enhance the risk of microbial pathogenesis. These factors have garnered significant interest. In this review, we summarise recent studies on the potential mechanisms involved in PM_2.5-mediated immune system disruption and exacerbation of microbial pathogenesis in the respiratory tract. We also discuss crucial areas for future research to address the gaps in our understanding and develop effective strategies to combat the adverse health effects of PM_2.5.

FIGURE 1

Particulate matter with a diameter ≤2.5 μm (PM_2.5) impairs immune function and promotes disease development. Schematic illustration of the mechanism underlying the suppression of the immune system mediated by PM_2.5. a) Representation of the respiratory system in a healthy individual and b) The airway status during PM_2.5 exposure. Upon exposure, PM_2.5 leads to mitochondrial dysfunction and induces reactive oxygen species (ROS) production in epithelial cells. Excessive ROS disrupts the integrity of the epithelial barrier and cilia, which impairs mucociliary clearance and allows bacteria to adhere to and colonise the upper respiratory tract. PM_2.5 even penetrates deeply into the lower respiratory tract to irradiate the alveolar epithelial cells and trigger ROS production. Injured alveolar epithelial cells and macrophages thereby produce proinflammatory cytokines and chemokines to recruit immune cells into the alveoli. However, the infiltration of immune cells into the alveoli exacerbates the lung damage. Meanwhile, monocyte-derived macrophages and T-cells further undergo polarisation in response to various costimulants, potentially resulting in alveolar fibrosis, lung adenocarcinoma or gas exchange failure. EGFR: epidermal growth factor receptor; IFN-β: interferon-β; IL: interleukin; IM: interstitial macrophage; MΦ: macrophage; PM₁₀: PM with a diameter ≤10 μm; Th: T-helper cell; TNF-α: tumour necrosis factor-α.