Spleen-derived classical monocytes mediate lung ischemia-reperfusion injury through IL-1β.

The Journal of Clinical Investigation
Hsi-Min HsiaoD Kreisel

Abstract

Ischemia-reperfusion injury, a form of sterile inflammation, is the leading risk factor for both short-term mortality following pulmonary transplantation and chronic lung allograft dysfunction. While it is well recognized that neutrophils are critical mediators of acute lung injury, processes that guide their entry into pulmonary tissue are not well understood. Here, we found that CCR2+ classical monocytes are necessary and sufficient for mediating extravasation of neutrophils into pulmonary tissue during ischemia-reperfusion injury following hilar clamping or lung transplantation. The classical monocytes were mobilized from the host spleen, and splenectomy attenuated the recruitment of classical monocytes as well as the entry of neutrophils into injured lung tissue, which was associated with improved graft function. Neutrophil extravasation was mediated by MyD88-dependent IL-1β production by graft-infiltrating classical monocytes, which downregulated the expression of the tight junction-associated protein ZO-2 in pulmonary vascular endothelial cells. Thus, we have uncovered a crucial role for classical monocytes, mobilized from the spleen, in mediating neutrophil extravasation, with potential implications for targeting of reci...Continue Reading

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Citations

Mar 26, 2019·American Journal of Respiratory Cell and Molecular Biology·Natalia F Smirnova, Oliver Eickelberg
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Methods Mentioned

BETA
flow cytometry
bronchoalveolar lavage
reverse-transcription PCR
transfection
PCR

Software Mentioned

GraphPad
AlphaEase imaging
Image Lab
Zeiss Efficient Navigation ZEN
ImageWarp

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