CD14(+) cells are necessary for increased survival of eosinophils in response to lipopolysaccharide

There has been considerable interest in the effect that gramnegative bacter ial endotoxin (lipopolysaccharide [LPS]) can have in asthma, given that inh alation of LPS has been shown to cause bronchial hyperresponsiveness. Furth er, there is evidence that the endotoxin-binding protein CD14 may be a mark er for asthma. Inhaled LPS has been shown to cause an influx of eosinophils into the nasal airway and to increase the survival of CD16-negatively sele cted eosinophils in vitro. In this study, we compared survival of eosinophi ls isolated via CD16-negative selection with eosinophils that were isolated using both CD16- and CD14-negative selection criteria. Survival of CD16-ne gatively selected eosinophils was enhanced by LPS in a dose-dependent manne r and was inhibited by the endotoxin antagonists polymyxin B or lipid X. In contrast, depletion of CD14(+) cells within the eosinophil preparations (C D14/CD16-negatively selected eosinophils) decreased the effect of LPS on su rvival. Preincubation of CD16-negatively selected eosinophils with antibody 60bd, which blocks LPS binding to CD14, prevented the survival-enhancing e ffect of LPS, However, CD14 was not detected on eosinophils by flow cytomet ry, even after incubation with LPS for up to 24 h, These results suggest th at the survival-enhancing effect of LPS on eosinophils requires the presenc e of CD14(+) cells in the population. It is our hypothesis that enhanced eo sinophil survival with LPS involves the contribution of another cell type.