Experimental models for investigating the influence of particulate matter with a diameter ≤2.5 μm (PM2.5) on bacterial infections
| Experimental platform | Pathogen | Immune response | Reference |
|---|---|---|---|
| PM2.5 suppresses immune response and exacerbates bacterial infection | |||
| Sprague–Dawley rats | Listeria monocytogenes | Exposure to diesel exhaust particles decreased the production of macrophage-derived antimicrobial oxidants in response to Listeria | [113] |
| BALB/c mice | Streptococcus pneumoniae | Soluble components of concentrated ambient particles inhibit the internalisation of Streptococcus pneumoniae by macrophages | [114] |
| A549 cells | Streptococcus pneumoniae | PM2.5 stimulates Streptococcus pneumoniae to adhere to respiratory epithelial cells | [115] |
| Sprague–Dawley rats | Klebsiella pneumoniae | PM2.5 impairs the bronchial ciliary system and the interaction of cytokines, increasing susceptibility to bacterial infection | [80] |
| Wistar rats | Staphylococcus aureus | PM2.5 downregulates macrophage phagocytosis and reduces pulmonary natural killer cells | [76] |
| Clinical study (a systemic review) | Mycobacterium tuberculosis | PM2.5 suppresses immune defence, increasing an individual's susceptibility to development of active TB and TB-related mortality | [78] |
| CD1, C57BL/6 and BALB/c mice | Streptococcus pneumoniae | PM loading of macrophages is associated with reduced phagocytic killing activity and promotes inflammation in the context of bacterial challenge | [75] |
| RAW 264.7 cells and BALB/c mice | Streptococcus pneumoniae | PM2.5 impedes the macrophage function to exacerbate bacterial infection | [59] |
| C57BL/6 mice | Pseudomonas aeruginosa | PM2.5 and Pseudomonas aeruginosa synergistically dampen alveolar macrophage function and induce inflammation through the mTOR pathway | [77] |
| PM2.5 enhances immune response and promotes inflammation | |||
| Clinical study (a systemic review) | Mycoplasma pneumoniae | The induction of oxidative stress mechanisms and the modulation of the host immune system are attributed to the interaction between PM2.5-associated metal complexes and Mycoplasma pneumoniae This interaction is assumed to occur through the TLRs and/or NF-κB pathway | [116] |
| RAW 264.7 cells and BALB/c mice | Pseudomonas aeruginosa | Co-stimulation with PM2.5 and Pseudomonas aeruginosa increases the expression of IL-8, IL-6 and TNF-α, leading to severe inflammation | [79] |
IL: interleukin; mTOR: mammalian target of rapamycin; TB: tuberculosis; TLR: Toll-like receptor; TNF-α: tumour necrosis factor-α.