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Napoli, M.* ; Immler, R.* ; Rohwedder, I.* ; Lupperger, V. ; Pfabe, J.* ; Gonzalez Pisfil, M.* ; Yevtushenko, A.* ; Vogl, T.* ; Roth, J.* ; Salvermoser, M.* ; Dietzel, S.* ; Slak Rupnik, M.* ; Marr, C. ; Walzog, B.* ; Sperandio, M.* ; Pruenster, M.*

Cytosolic S100A8/A9 promotes Ca2+ supply at LFA-1 adhesion clusters during neutrophil recruitment.

eLife 13:RP96810 (2024)
Verlagsversion DOI PMC
Open Access Gold
Creative Commons Lizenzvertrag
S100A8/A9 is an endogenous alarmin secreted by myeloid cells during many acute and chronic inflammatory disorders. Despite increasing evidence of the proinflammatory effects of extracellular S100A8/A9, little is known about its intracellular function. Here, we show that cytosolic S100A8/A9 is indispensable for neutrophil post-arrest modifications during outside-in signaling under flow conditions in vitro and neutrophil recruitment in vivo, independent of its extracellular functions. Mechanistically, genetic deletion of S100A9 in mice caused dysregulated Ca2+ signatures in activated neutrophils resulting in reduced Ca2+ availability at the formed LFA-1/F-actin clusters with defective β2 integrin outside-in signaling during post-arrest modifications. Consequently, we observed impaired cytoskeletal rearrangement, cell polarization, and spreading, as well as cell protrusion formation in S100a9-/- compared to wildtype (WT) neutrophils, making S100a9-/- cells more susceptible to detach under flow, thereby preventing efficient neutrophil recruitment and extravasation into inflamed tissue.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Lfa-1 Integrin Clustering ; Acute Inflammation ; Calcium Signaling ; Immunology ; Inflammation ; Intracellular S100a8/a9 ; Intracellular Signaling ; Mouse ; Neutrophil Recruitment; Leukocyte Recruitment; Molecular-mechanisms; Calcium Flux; Activation; Mrp14; Arrest; Polarization; Migration; Orai1
Sprache englisch
Veröffentlichungsjahr 2024
HGF-Berichtsjahr 2024
ISSN (print) / ISBN 2050-084X
e-ISSN 2050-084X
Zeitschrift eLife
Quellenangaben Band: 13, Heft: , Seiten: , Artikelnummer: RP96810 Supplement: ,
Verlag eLife Sciences Publications
Verlagsort 95 Regent Street, Cambridge, England
Begutachtungsstatus Peer reviewed
Institut(e) Institute of AI for Health (AIH)
POF Topic(s) 30205 - Bioengineering and Digital Health
Forschungsfeld(er) Enabling and Novel Technologies
PSP-Element(e) G-540007-001
Förderungen Deutsche Forschungsgemeinschaft
DOI 10.7554/eLife.96810
WOS ID 001394410200001
Scopus ID 85213188452
PubMed ID 39699020
Erfassungsdatum 2024-12-20
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