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Applied Pharmacology and
Unit of Critical Care, National Heart and Lung Institute Division, Imperial College School of Medicine, London, United Kingdom; and
Section of Vascular Biology, University of Sheffield, Clinical Sciences Centre, Northern General Hospital, Sheffield, United Kingdom
Cell adhesion molecule expression (CAM) and IL-8 release in lung
microvascular endothelium facilitate neutrophil accumulation in the
lung. This study investigated the effects of lipoteichoic acid (LTA), a
cell wall component of Gram-positive bacteria, alone and with LPS or
TNF-
, on CAM expression and IL-8 release in human lung microvascular
endothelial cells (HLMVEC). The concentration-dependent effects of
Staphylococcus aureus (S. aureus) LTA (0.3–30 µg/ml)
on ICAM-1 and E-selectin expression and IL-8 release were bell shaped.
Streptococcus pyogenes (S. pyogenes) LTA had no effect
on CAM expression, but caused a concentration-dependent increase in
IL-8 release. S. aureus and S. pyogenes
LTA (30 µg/ml) abolished LPS-induced CAM expression, and S.
aureus LTA reduced LPS-induced IL-8 release. In contrast, the
effects of S. aureus LTA with TNF- on CAM expression
and IL-8 release were additive. Inhibitory effects of LTA were not due
to decreased HLMVEC viability, as assessed by ethidium homodimer-1
uptake. Changes in neutrophil adhesion to HLMVEC paralleled changes in
CAM expression. Using RT-PCR to assess mRNA levels, S.
aureus LTA (3 µg/ml) caused a protein synthesis-dependent
reduction (75%) in LPS-induced IL-8 mRNA and decreased the IL-8 mRNA
half-life from >6 h with LPS to 
2 h. These results suggest that
mechanisms exist to prevent excessive endothelial cell activation in
the presence of high concentrations of bacterial products. However,
inhibition of HLMVEC CAM expression and IL-8 release ultimately may
contribute to decreased neutrophil accumulation, persistence of
bacteria in the lung, and increased severity of
infection.
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