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Lung ICAM-1 and ICAM-2 support spontaneous intravascular effector lymphocyte entrapment but are not required for neutrophil entrapment or emigration inside endotoxin-inflamed lungs
Weizmann Inst Sci, Dept Immunol, IL-76100 Rehovot, Israel..
Weizmann Inst Sci, Dept Immunol, IL-76100 Rehovot, Israel..
Weizmann Inst Sci, Dept Immunol, IL-76100 Rehovot, Israel..
Weizmann Inst Sci, Dept Immunol, IL-76100 Rehovot, Israel..
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2016 (English)In: The FASEB Journal, ISSN 0892-6638, E-ISSN 1530-6860, Vol. 30, no 5, 1767-1778 p.Article in journal (Refereed) Published
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Abstract [en]

The pulmonary vasculature constitutively expresses the integrin lymphocyte function-associated antigen-1 ligands intercellular adhesion molecule (ICAM)-1 and -2. In this study, effector T cells were temporarily entrapped by the lung vasculature on their way to inflamed lymph nodes, and this entrapment was strongly reduced in ICAM-1 and -2 double-deficient mice (79 and 86% reduction for CD8(+) and CD4(+) effectors, respectively, compared with wild-type mice). Although the pulmonary vasculature has been suggested to be masked by the heparan sulfate-containing glycocalyx, which is susceptible to heparanase-mediated shedding, lung and lymphocyte heparanase have been found to be unnecessary for this entrapment. Systemic LPS induced rapid neutrophil entrapment in the lung vasculature, but in contrast to T-cell entrapment, this sequestration was ICAM-1, ICAM-2, and heparanase independent. Furthermore, neutrophil migration into the bronchoalveolar space induced by LPS inhalation and LPS-induced leakage of red blood cells into this space were not dependent on lung ICAMs or heparanase activity. Nevertheless, heparanase was critical for neutrophil accumulation in smoke-exposed lungs. Our results indicate that, whereas T cells use ICAM-1 and -2 for temporary pulmonary entrapment, neutrophils get sequestered and extravasate into inflamed lungs independent of ICAMs. This is the first demonstration that the pulmonary vasculature is differentially recognized by T cells and neutrophils.-Petrovich, E., Feigelson, S. W., Stoler-Barak, L., Hatzav, M., Solomon, A., Bar-Shai, A., Ilan, N., Li, J.-P., Engelhardt, B., Vlodavsky, I., Alon, R. Lung ICAM-1 and ICAM-2 support spontaneous intravascular effector lymphocyte entrapment but are not required for neutrophil entrapment or emigration inside endotoxin-inflamed lungs.

Place, publisher, year, edition, pages
2016. Vol. 30, no 5, 1767-1778 p.
Keyword [en]
beta(2) integrin, heparanase, heparan sulfate, inflammation
National Category
Medical and Health Sciences
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URN: urn:nbn:se:uu:diva-297288DOI: 10.1096/fj.201500046ISI: 000374879400008PubMedID: 26823454OAI: oai:DiVA.org:uu-297288DiVA: diva2:941450
Available from: 2016-06-22 Created: 2016-06-22 Last updated: 2016-06-22Bibliographically approved

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