Underground railway particulate matter and susceptibility to pneumococcal infection.

Abstract

Concentrations of particulate matter less than 10 microns (PM₁₀) on underground railways are higher than those near urban roads. Traffic-related PM₁₀ increases pneumococcal infection via increasing the expression of platelet-activating factor receptor (PAFR), a receptor co-opted by pneumococci to adhere to cells. To date, it is unknown whether underground railway PM₁₀ increases pneumococcal infection. This study sought to determine the effect of London Underground (LU) PM₁₀ on; i) pneumococcal adhesion to airway cells, and ii) susceptibility to pneumococcal disease. A549 cells and human primary airway epithelial cells were cultured with 20 µg/mL PM₁₀ from the Bakerloo (B-PM₁₀) and Jubilee (J-PM₁₀) line platforms of Baker Street station. PAFR expression was assessed by flow cytometry, and pneumococcal adhesion by colony forming unit (CFU) counts. Traffic-related PM₁₀ was collected next to a main road near the station's entrance. The PAFR blocker CV3988 and the antioxidant N-acetyl cysteine were used to assess the role of PAFR-mediated pneumococcal adhesion and oxidative stress respectively. Pneumococcal infection of mice was done after exposure to 3×80 μg doses of intranasal LU-PM₁₀. In A549 cells, human primary nasal cells, and human primary bronchial epithelial cells, B-PM₁₀ and J-PM₁₀ increased PAFR expression and pneumococcal adhesion. Stimulated adhesion was abrogated by CV3988 and N-acetyl cysteine. Traffic-related PM₁₀ stimulated increased adhesion compared with B-PM₁₀. B-PM₁₀ and J-PM₁₀ increased lung and blood CFU and mortality in mice. Treatment of B-PM₁₀-exposed mice with CV3988 reduced blood CFU. LU-PM₁₀ increases pneumococcal adhesion to airway cells and susceptibility to invasive disease in mice. The Medical College of Saint Bartholomew's Hospital Trust, and the UK Medical Research Council Programme Grant (MR/P011284/1).