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Abstract

We have studied the expression of the lipopolysaccharide (LPS) receptor CD14 on monocytes (Mo) and alveolar macrophages (AM), including density- and size-defined subpopulations. Bronchoalveolar lavage (BAL) was performed on eleven healthy non-smokers and blood sampled from 5 of them, and the levels of cell CD14 expression was investigated using flow cytometry. The influence of LPS stimulation on the CD14 expression of AM was studied at various intervals during prolonged incubation. Further, the relationship between CD14 expression and LPS binding to Mo and subpopulations of AM was studied by measuring fluorescein isothiocyanate (FITC)-LPS binding (flow cytometry) and binding of radioiodinated LPS (125I-LPS). The CD14 expression was 13-fold higher (P < 0.02) on Mo than on unfractionated and high density AM. The CD14 level on the latter was higher than on low density AM, and also higher (P < 0.05) on small AM compared to large (flow cytometrically defined) AM. LPS stimulation had a downregulating effect on AM CD14 level, but after several hours of continuing decreased expression, an increased (P < 0.05) CD14 expression was demonstrated, indicating de novo synthesis. The binding of LPS to subpopulations of AM and isolated Mo was not significantly different, but the binding of FITC-LPS to Mo in whole blood was higher than to AM (P < 0.02). The presented results indicate that AM of different size and maturity have different and variable (activation dependent) CD14 levels. The LPS binding capacity was, however, not proportional to the CD14 expression, indicating that LPS binding mechanisms unrelated to CD14 levels were also operable.

Differential cell reaction upon Toll-like receptor 4 and 9 activation in human alveolar and lung interstitial macrophages

“…We were able to show that CD14 is marginally expressed in human AM as well as IM. Low CD14 expression was reported previously for human AM obtained from bronchoalveolar lavage [28,29]. CD14 expression by human IM is not described in the literature, but our results resemble findings reported for other tissue macrophage populations [28].…”

Lysophosphatidylcholine Acetyltransferase 2 (LPCAT2) Influences the Gene Expression of the Lipopolysaccharide Receptor Complex in Infected RAW264.7 Macrophages, Depending on the E. coli Lipopolysaccharide Serotype

“…Scientific evidence shows CD14 is vital for TLR4 signalling via the MyD88independent pathway [38]. As the results described in this paper confirm, CD14 gene expression is increased by LPS in alveolar macrophages after several hours of infection [39], TLR4 gene expression is decreased by LPS infection of mouse macrophages [40], and MD2 gene expression is higher after LPS infection of alveolar macrophages [41]. Furthermore, our data show, in Figures 3 and 4, that LPCAT2 regulated these molecules' gene expression, albeit only in non-infected and E. coli O111:B4-infected macrophages.…”

Expression, regulation and clinical significance of soluble and membrane CD14 receptors in pediatric inflammatory lung diseases

“…Alexis et al demonstrated that neutrophil elastase reduced CD14 expression on alveolar phagocytes in vitro , which might represent the underlying cause for the low mCD14 expression on CF alveolar macrophages [32,33]. Two previous studies demonstrated that short-term incubation with LPS decreased mCD14, whereas long-term LPS treatment resulted in increased mCD14 expression on monocytes [21] and alveolar macrophages [34]. Our findings indicate that 40 h incubation with LPS and CpG induced sCD14 secretion and increased mCD14 expression of PBMCs.…”