Regulation of ICAM-1 in human neutrophils.

Autor:	Vignarajah M; Wolfson Foundation Lung Injury Unit, Victor Phillip Dahdaleh Heart and Lung Research Institute, University of Cambridge School of Clinical Medicine, Papworth Road, Cambridge, CB2 0BB, United Kingdom., Wood AJT; Wolfson Foundation Lung Injury Unit, Victor Phillip Dahdaleh Heart and Lung Research Institute, University of Cambridge School of Clinical Medicine, Papworth Road, Cambridge, CB2 0BB, United Kingdom., Nelmes E; Wolfson Foundation Lung Injury Unit, Victor Phillip Dahdaleh Heart and Lung Research Institute, University of Cambridge School of Clinical Medicine, Papworth Road, Cambridge, CB2 0BB, United Kingdom., Subburayalu J; Wolfson Foundation Lung Injury Unit, Victor Phillip Dahdaleh Heart and Lung Research Institute, University of Cambridge School of Clinical Medicine, Papworth Road, Cambridge, CB2 0BB, United Kingdom., Herre J; Department of Respiratory Medicine, Cambridge University Hospitals NHS Foundation Trust, Hills Road, Cambridge, CB2 0QQ, United Kingdom., Nourshargh S; William Harvey Research Institute, Faculty of Medicine and Dentistry, Queen Mary University of London, Charterhouse Square, London, EC1M 6BQ, United Kingdom., Summers C; Wolfson Foundation Lung Injury Unit, Victor Phillip Dahdaleh Heart and Lung Research Institute, University of Cambridge School of Clinical Medicine, Papworth Road, Cambridge, CB2 0BB, United Kingdom., Chilvers ER; National Heart and Lung Institute, Imperial College London, 72 Du Cane Rd, London, W12 0NN, United Kingdom., Farahi N; Wolfson Foundation Lung Injury Unit, Victor Phillip Dahdaleh Heart and Lung Research Institute, University of Cambridge School of Clinical Medicine, Papworth Road, Cambridge, CB2 0BB, United Kingdom.
Jazyk:	angličtina
Zdroj:	Journal of leukocyte biology [J Leukoc Biol] 2024 Oct 01; Vol. 116 (4), pp. 901-908.
DOI:	10.1093/jleuko/qiae090
Abstrakt:	Intercellular cell adhesion molecule 1 (ICAM-1) is a cell surface glycoprotein with a vital role in the immune response to pathogens. The expression pattern of ICAM-1 is wide ranging, encompassing endothelial cells, epithelial cells, and neutrophils. Recent work has characterized the role of ICAM-1 in murine neutrophils, but the function of human neutrophil ICAM-1 is incompletely understood. Herein, we investigated the expression and role of ICAMs in human neutrophils in vitro and in vivo. Our findings show clear expression of ICAM-1, -3, and -4 on peripheral blood-derived neutrophils and demonstrate that the pathogen-associated molecular pattern lipoteichoic acid is an inducer of ICAM-1 expression in vitro. In vivo, neutrophils obtained from the pleural cavity of patients with a parapneumonic effusion display enhanced expression of ICAM-1 compared with peripheral blood- and oral cavity-derived neutrophils. Moreover, migration of peripheral blood-derived neutrophils across endothelial cells can upregulate neutrophil ICAM-1 expression. These findings indicate that pathogen-associated molecular patterns and/or cytokines, alongside transmigration, enhance neutrophil ICAM-1 expression at sites of inflammation. Mechanistically, we observed that ICAM-1high neutrophils display elevated S. aureus phagocytic capacity. However, unlike murine neutrophils, ICAM-1 intracellular signaling in human neutrophils was not essential for phagocytosis of Staphylococcus aureus and reactive oxygen species generation. Taken together, these results have important implications for the regulation of neutrophil-mediated pathogen clearance. (© The Author(s) 2024. Published by Oxford University Press on behalf of Society for Leukocyte Biology.)
Databáze:	MEDLINE
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