RT Journal Article
SR Electronic
T1 Streptococcus pneumoniae inhibits Pseudomonas aeruginosa growth on nasal human epithelium in vitro
JF European Respiratory Journal
JO Eur Respir J
FD European Respiratory Society
SP PA5455
DO 10.1183/13993003.congress-2018.PA5455
VO 52
IS suppl 62
A1 Song Huang
A1 Carole Bertinetti
A1 Ophélie Verbeke
A1 Mireille Caul-Futy
A1 Paul Alouani
A1 Ludovic Wiszniewski
A1 Samuel Constant
YR 2018
UL http://erj.ersjournals.com/content/52/suppl_62/PA5455.abstract
AB Pathogens colonizing the respiratory tract compete with a range of other bacteria (1). Pseudomonas aeruginosa (PA) infection are increasingly associated with acute exacerbations in chronic obstructive pulmonary disease. Streptococcus pneumoniae (SP), meanwhile is a main cause of pneumonia, meningitis, it can leads to infections and other respiratory diseases such as bronchitis.We report herein the use of 3D airway epithelia reconstituted in vitro to study interactions of PA and SP on nasal mucosa. MucilAir™, a fully differentiated human airway epithelium made of a mixture of primary nasal cells from 14 donors, was used to study the effects and behaviour of PA and SP (inoculated at 3E+02 and 3E+11 CFU/cm2 respectively) cultivated separately or together over 24 hours.Apical, basolateral and intratissular PA and SP growth were quantified by Colony Forming Unit (CFU). Impairment of epithelial homeostatic barrier function was evaluated through monitoring of tissue integrity (Trans Epithelial Electrical Resistance – TEER); cytotoxicity (LDH), cilia activity, mucin and IL-8 release.PA infection induces a loss of TEER, 20% cytotoxicity and an increase of Il-8 (+100 ng/ml). On the contrary, SP strongly increases the mucin production. While inoculated together, a lower apical PA growth is observed (- 3E+3 CFU/cm2) suggesting an inhibition due to the presence of SP.These results suggest that in vitro human airway epithelia is a useful model to study bacterial interaction on the human nasal mucosa.[1] Siegel, S.J.; Weiser, J.N. Annu Rev Microbiol. 2015 ; 69: 425–444FootnotesCite this article as: European Respiratory Journal 2018 52: Suppl. 62, PA5455.This is an ERS International Congress abstract. No full-text version is available. Further material to accompany this abstract may be available at www.ers-education.org (ERS member access only).