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. 2019 Oct 1;10:2320. doi: 10.3389/fimmu.2019.02320

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Copyright © 2019 Erpenbeck, Gruhn, Kudryasheva, Günay, Meyer, Busse, Neubert, Schön, Rehfeldt and Kruss.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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PI3K inhibition impairs neutrophil adhesion and affects NETosis in a stimulant-dependent manner. Human neutrophils were seeded on fibrinogen-coated PAA gels (4 and 128 kPa) and glass (serving as a control) and the spreading area was quantified with and without PI3K inhibition after 30 min (A,B). Representative phase contrast images are shown in (A). PI3K inhibition leveled out the elasticity-dependent differences in cell contact area. Then NETosis was induced by PMA (5 nM) (C) or LPS (75 μg/mL) (D) and quantified after 3 h. LPS-induced NETosis is completely abolished. In contrast, PMA-induced NETosis is only partially reduced by PI3K inhibition. n > 500 cells per condition. N = 3 donors. Mean ± SEM of independent donors. Statistics: one-way ANOVA (Bonferroni's multiple comparisons test. *p < 0.05; ****p < 0.0001; ns: not significant).