Adhesion of Streptococcus pneumoniae to human airway epithelial cells exposed to urban particulate matter.
BACKGROUND
Epidemiologic studies report an association between pneumonia and urban particulate matter (PM) less than 10 microns (μm) in aerodynamic diameter (PM(10)). Streptococcus pneumoniae is a common cause of bacterial pneumonia worldwide. To date, the mechanism whereby urban PM enhances vulnerability to S pneumoniae infection is unclear. Adhesion of S pneumoniae to host cells is a prerequisite for infection. Host-expressed proteins, including the receptor for platelet-activating factor (PAFR), are co-opted by S pneumoniae to adhere to lower airway epithelial cells.


OBJECTIVE
To define whether inhalable urban PM enhances the adhesion of S pneumoniae to airway epithelial cells.


METHODS
A549 cells were cultured with PM(10) from Leicester (United Kingdom [UK]) and PM(10) and PM less than 2.5 μm in aerodynamic diameter (PM(2.5)) from Accra (Ghana), then infected with S pneumoniae strain D39. Pneumococcal adhesion to human primary bronchial epithelial cells was also assessed. Bacterial adhesion was determined by quantitative culture and confocal microscopy. The role of oxidative stress was assessed by N-acetyl cysteine, and the role of PAFR was assessed by mRNA transcript level, receptor expression, and receptor blocking.


RESULTS
PM(10) (UK) increased S pneumoniae adhesion to both A549 airway epithelial cells and human primary bronchial epithelial cells. PM(10) (Ghana) and PM(2.5) (Ghana) also increased adhesion. Culture of A549 cells by PM(10) (UK) increased PAFR mRNA transcript level and PAFR expression. PM(10) (UK)-stimulated adhesion to A549 cells was attenuated by a PAFR blocker and N-acetyl cysteine.


CONCLUSIONS
Urban PM increases adhesion of S pneumoniae to human airway epithelial cells. PM-stimulated adhesion is mediated by oxidative stress and PAFR.
Blizard Institute of Cell and Molecular Science, Barts and the London School of Medicine and Dentistry, Queen Mary University London, London, United Kingdom.
Naseem
N
Mushtaq
Majid
M
Ezzati
Lucinda
L
Hall
Iain
I
Dickson
Michael
M
Kirwan
Ken M Y
KM
Png
Ian S
IS
Mudway
Jonathan
J
Grigg
D001422:Bacterial Adhesion / Q000187:drug effects* / Q000502:physiology*; D002460:Cell Line; D004847:Epithelial Cells / Q000166:cytology / Q000187:drug effects / Q000382:microbiology*; D005869:Ghana; D006801:Humans; D018384:Oxidative Stress; D052638:Particulate Matter / Q000378:metabolism / Q000494:pharmacology*; D010972:Platelet Activating Factor / Q000235:genetics / Q000378:metabolism; D010980:Platelet Membrane Glycoproteins / Q000235:genetics / Q000378:metabolism*; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D043562:Receptors, G-Protein-Coupled / Q000235:genetics / Q000378:metabolism*; D012137:Respiratory System / Q000166:cytology* / Q000187:drug effects / Q000382:microbiology; D013296:Streptococcus pneumoniae / Q000502:physiology*; D006113:United Kingdom
D052638:Particulate Matter; D010972:Platelet Activating Factor; D010980:Platelet Membrane Glycoproteins; D012333:RNA, Messenger; D043562:Receptors, G-Protein-Coupled; C039351:platelet activating factor receptor