“…For NET blockage, the following inhibitors were used: the NOX-inhibitor DPI [10 µM, Sigma-Aldrich, according to Farley et al (43)], the leukocyte elastase-inhibitor Suc-Ala-Ala-Pro-Val chloromethyl ketone [CMK; 1 mM, Sigma-Aldrich, according to Scapinello et al (44)], the MPO-inhibitor 4-aminobenzoic acid hydrazide [ABAH; 100 µM, Merck, according Parker et al (45)], the SOCE-inhibitor aminoethoxydiphenyl borate [2-APB; 100 µM, Sigma-Aldrich, according to Conejeros et al (46)], UO126 as inhibitor of ERK1/2 [50 µM; Sigma-Aldrich, according to Muñoz-Caro et al (12)], SB 202190 as specific inhibitor of p38 MAPK [10 µM; Sigma-Aldrich, according to Muñoz-Caro et al (12)], the G-protein-coupled receptor (GPCR) antagonist NF-449 for P2Y2 blockage (GPCR-NF-449, 10 µM; Santa Cruz Biotechnology), and N-α-benzoyl-N5-(2-chloro-1-iminoethyl)- l -Orn amide for PAD4 inhibition (Cl-amidine, 200 µM, Merck). For blocking experiments, PMN were pre-exposed with the corresponding inhibitor in serum-free medium RPMI 1640 without phenol red (RT, GPCR-NF-449, and Cl-amidine: 120 min, all other inhibitors: 30 min) prior to exposure to N. caninum tachyzoites.…”