RT Journal Article
SR Electronic
T1 Lipopolysaccharide-binding protein and CD14 are increased in the bronchoalveolar lavage fluid of smokers
JF European Respiratory Journal
JO Eur Respir J
FD European Respiratory Society
SP 273
OP 281
DO 10.1183/09031936.00087708
VO 33
IS 2
A1 Regueiro, V.
A1 Campos, M. A.
A1 Morey, P.
A1 Sauleda, J.
A1 Agustí, A.G.N.
A1 Garmendia, J.
A1 Bengoechea, J. A.
YR 2009
UL http://erj.ersjournals.com/content/33/2/273.abstract
AB Lipopolysaccharide-binding protein (LBP) and CD14 contribute to the recognition of pathogens by cells, which triggers the activation of defence responses. Smoking is a risk factor for the development of chronic obstructive pulmonary disease (COPD) and respiratory infections. The current authors theorised that levels of LBP and CD14 in the lungs of smokers would be higher than those in the lungs of never-smokers. These elevated levels could affect host responses upon infection. LBP, soluble CD14 (sCD14) and interleukin (IL)-8 were detected by ELISA. Nuclear factor (NF)-κB, p38 and the inhibitor IκBα were studied by immunoassays. Gene expression was assessed by RT-PCR. Bronchoalveolar lavage levels of LBP and CD14 were significantly higher in smokers and COPD patients than in never-smokers, whereas levels of both proteins were not significantly different between smokers and COPD patients. IL-6, IL-1β and cigarette smoke condensate induced the expression of LBP and CD14 by airway epithelial cells. LBP and sCD14 inhibited the nontypeable Haemophilus influenzae (NTHi)-dependent secretion of IL-8 and the activation of NF-κB and p38 mitogen-activated protein kinase signalling pathways but they increased the internalisation of NTHi by airway epithelial cells. Thus, in the inflamed airways of smokers both proteins could contribute to inhibit bacteria-dependent cellular activation without compromising the internalisation of pathogens by airway cells.