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CorrigendumAging Free access | 10.1172/JCI16510C1

Endothelium-derived Toll-like receptor-4 is the key molecule in LPS-induced neutrophil sequestration into lungs

Graciela Andonegui, Claudine S. Bonder, Francis Green, Sarah C. Mullaly, Lori Zbytnuik, Eko Raharjo, and Paul Kubes

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Published October 15, 2003 - More info

Published in Volume 112, Issue 8 on October 15, 2003
J Clin Invest. 2003;112(8):1264–1264. https://doi.org/10.1172/JCI16510C1.
© 2003 The American Society for Clinical Investigation
Published October 15, 2003 - Version history
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Endothelium-derived Toll-like receptor-4 is the key molecule in LPS-induced neutrophil sequestration into lungs
Graciela Andonegui, … , Eko Raharjo, Paul Kubes
Graciela Andonegui, … , Eko Raharjo, Paul Kubes
Article Aging

Endothelium-derived Toll-like receptor-4 is the key molecule in LPS-induced neutrophil sequestration into lungs

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Abstract

The rapid and selective accumulation of neutrophils into the lungs is thought to underlie the pulmonary failure that leads to sepsis-related death. In this study we investigated whether neutrophil TLR4 is important in LPS-induced pulmonary neutrophil recruitment by creating chimeric mice (transferring bone marrow between TLR4+/+ and TLR4–/– mice). In TLR4+/+ mice receiving TLR4–/– bone marrow, 6 weeks after transplant TLR4 was absent in all circulating leukocytes as well as in resident macrophages (these mice were termed LeukocyteTLR4–/–), and these cells were completely nonresponsive to LPS. In TLR4–/– mice receiving TLR4+/+ bone marrow, endothelial cells but not leukocytes were deficient in TLR4 (EndotheliumTLR4–/–). Surprisingly, systemic LPS (0.5 mg/kg) induced a dramatic increase in neutrophil sequestration into the lungs of LeukocyteTLR4–/– mice over the first 4 hours. Concomitantly, numbers of circulating leukocytes decreased by 90%. By contrast, EndotheliumTLR4–/– mice showed very little increase in neutrophil sequestration in the lungs, suggesting that endothelium rather than leukocyte TLR4 was important. Intravital microscopy of peripheral microcirculation in the cremaster muscle revealed about 30-fold more leukocyte–endothelial cell interactions in LPS-treated EndotheliumTLR4–/– mice than in LPS-treated LeukocyteTLR4–/– mice. This is consistent with less sequestration of leukocytes into the lungs of EndotheliumTLR4–/– mice. In conclusion, our data challenge the view that LPS directly activates neutrophils to trap in lungs and suggest a far more important role than previously appreciated for the endothelial cells.

Authors

Graciela Andonegui, Claudine S. Bonder, Francis Green, Sarah C. Mullaly, Lori Zbytnuik, Eko Raharjo, Paul Kubes

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Original citation: J. Clin. Invest.112:1011–1020 (2003). doi:10.1172/JCI16510.

Citation for this erratum: J. Clin. Invest.112:1264 (2003). doi:10.1172/JCI16510C1.

On pages 1012 and 1015, The authors inadvertently referred to the mice lacking the TLR4 gene obtained from The Jackson Laboratory as generated TLR4 knockout mice. These mice are the naturally occurring knockout or null mutant (TLR4LPS-del) mice from The Jackson Laboratory, which, nevertheless, lack the gene, message, and protein.

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