E-cigarette vapour enhances pneumococcal adherence to airway epithelial cells

Area of Science:

• Respiratory Medicine
• Microbiology
• Toxicology

Background:

• E-cigarette vapor contains free radicals, inducing oxidative stress.
• Oxidative stress elevates airway cell platelet-activating factor receptor (PAFR) expression.
• PAFR is crucial for pneumococcal adherence to host cells.

Purpose of the Study:

• To investigate if E-cigarette vapor increases pneumococcal adhesion to airway cells.
• To determine the role of PAFR and oxidative stress in this process.
• To assess the impact of vaping on pneumococcal colonization in vivo.

Main Methods:

• Assessed nasal epithelial PAFR in controls and vapers before/after vaping.
• Measured in vitro pneumococcal adhesion to airway cells exposed to vapor.
• Analyzed vapor composition and oxidative potential.
• Evaluated in vivo pneumococcal colonization in a mouse model.

Main Results:

• Vaping increased nasal epithelial PAFR expression.
• E-cigarette vapor (nicotine and nicotine-free) enhanced pneumococcal adhesion in vitro, blocked by a PAFR antagonist.
• Vapor exhibited oxidative activity and contained redox-active metals.
• Vaping increased pneumococcal colonization in mouse nasopharynx.
• Antioxidants attenuated vapor-induced adhesion.

Conclusions:

• E-cigarette vapor elevates PAFR expression and oxidative stress.
• Vaping promotes pneumococcal adhesion and colonization.
• This suggests E-cigarette use may increase susceptibility to pneumococcal infections.