Background and Objectives Epidemiological studies suggest that that occupational exposure to welding fumes (WF), increases susceptibility to invasive pneumococcal disease.1 The alveoli are a site for invasive disease caused by Streptococcus pneumoniae (Sp). To date the mechanism whereby welding fumes increases susceptibility to pneumococcal pneumonia is unknown. Platelet activating factor receptor (PAFR) is a host entry receptor for Sp in airway cells exposed to particulate matter air pollution.2 We assessed the hypothesis that welding fumes increase adhesion of Sp to airway cells via PAFR.
Methods Fume from a mild steel hyperbaric welding operation (WF) were collected from filtres and resuspended in PBS. Monolayers of the alveolar epithelial cell line, A549, were exposed to either WF alone or WF + a PAFR blocker (CV3988) for 3 h. Cells were then exposed to Sp for 2 h. Adherent and internalised bacteria were assessed by quantitative culture. Data were expressed as a mean±SEM of >4 replicates and were compared by t test.
Conclusion Increased PAFR-medicated pneumococcaladhesion to lower airway cells is a putative mechanism for the association between exposure to WF and vulnerability to pneumococcal pneumonia.
Palmer, KT; Poole, J; Ayres, J G; Mann, J; Burge, P S; Coggon, D. Exposure to Metal Fume and Infectious Pneumonia. American Journal of Epidemiology 157, 227–233 (2003).
Mushtaq, N et al. Adhesion ofStreptococcus pneumoniae to human airway epithelial cells exposed to urbanparticulate matter. The Journal of allergy and clinical immunology 127,1236–42 (2011).
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