LBP and CD14 are increased in the bronchoalveolar lavage fluid of smokers

¹ Centro Investigación Biomédica en Red de Enfermedades Respiratorias (CibeRes), Bunyola; and Program Infection and Immunity, Fundación Caubet-CIMERA Illes Balears, Bunyola
² Centro Investigación Biomédica en Red de Enfermedades Respiratorias (CibeRes), Bunyola; Program Infection and Immunity, Fundación Caubet-CIMERA Illes Balears, Bunyola; and Servicio de Neumología, Hospital Universitari Son Dureta, Palma Mallorca; Spain

^* To whom correspondence should be addressed. E-mail: bengoechea{at}caubet-cimera.es.

	Abstract

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 infections. We theorized that levels of LBP and CD14 in the lungs from smokers would be higher than those in the lungs from never smokers. These elevated levels could affect host responses upon infection.

LBP, sCD14, IL-8 were detected by ELISA. NF-B, p38 and IB were studied by immunoassays. Gene expression was assessed by RT-PCR.

Broncho-alveolar 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 in smokers and COPD patients. IL-6 and IL-1 and cigarette smoke condensate induced the expression of LBP and CD14 by airway epithelial cells. LBP and sCD14 inhibited the nontypable Haemophilus influenzae (NTHi)-dependent secretion of IL-8 and the activation of NF-B and p38 MAP 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.

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