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Bacterial lipoprotein delays neutrophil apoptosis via a CD14‐independent pathway.

Published: 6th December 2002

Authors: C. Power, J. H. Wang, S. Blankson, W. O. Kirwan, H. P. Redmond

Background

Lipopolysaccharide (LPS) is considered the most potent exogenous mediator of the systemic inflammatory response syndrome (SIRS) which results, in part, from delayed neutrophil (PMN) apoptosis. The effects of another ubiquitous bacterial component, bacterial lipoprotein (BLP), the most abundant protein in the cell wall of all bacteria, on PMN apoptosis are unknown. The potential role of BLP in the regulation of PMN apoptosis was investigated and these effects were compared with those of LPS.

Method

PMNs from healthy volunteers were isolated and exposed to identical concentrations of LPS and BLP in the presence or absence of recombinant antihuman CD14 monoclonal antibody. PMN apoptosis was assessed 6 hourly using Annexin V–propidium iodide staining and confirmed on cell morphology. PNM activation was assessed flow cytometrically using expression of functional markers CD11b and CD18.

Results

BLP significantly delayed PMN apoptosis and upregulated PMN adhesion receptor expression compared with control values. The effects seen were markedly similar to those of LPS.














PMN apoptosis (%)


Control
BLP (μg)
LPS (μg)


10
100
1000
10
100
1000




6 h
11
8*
7*
6*
7*
6*
7*


12 h
24
12*
10*
8*
9*
8*
9*


18 h
41
26*
17*
18*
15*
16*
15*


24 h
53
36*
31*
31*
27*
27*
28*






Values are mean(s.d.).

Conclusion

BLP is capable of upregulating PMN adhesion receptor expression and delaying PMN apoptosis in a time‐ and dose‐dependent manner independent of CD14. The potency, and the effects mediated by, BLP are very similar to those of LPS. This identifies BLP as a putative mediator of SIRS and demands that due attention be paid to other bacterial products in the investigation and treatment of septic states. © 2000 British Journal of Surgery Society Ltd

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