Fig. 6: Inhibition of ROS pathway abrogates the pro-metastatic and anti-metastatic effects of neutrophils in vivo.

a–e ROS blockade reversed neutrophilia-induced NK cell suppression. As depicted in a, ROS inhibitor HDC or the vehicle control was given to the NOD-scid mice bearing E0771 or E0771-g-csf orthotopic tumors at the pre-metastatic stage (day 8 and 10). On day 11, the mouse lungs were isolated for ROS level determination by bioluminescence (probe L-012) (b), total lung-infiltrating NK cell counting (c), and measurement of IFNγ⁺ NK cells (d) and CD107a⁺ NK cells (e) by flow cytometry. n = 5 mice per group. f–i Administration of the ROS inhibitor HDC abolished the tumor cell G-csf overexpression-induced metastases-regulatory effects. As depicted in f, h, NOD-scid (g) or NSG (i) mice were first orthotopically injected with unlabeled E0771 and E0771-g-csf cells to generate the non-inflammatory and inflammatory host conditions, respectively. E0771-Luc cells were i.v. infused at the pre-metastatic stage (day 10). From day 8, the mice also received HDC (1mg per mouse) every other day. At the endpoint, the metastatic progression of E0771-Luc cells in the lungs was detected by ex vivo BLI. The bioluminescence images (left) and the quantification of photon flux of lungs (right) are shown (g, i). n = 6 mice per group. Data are represented as mean ± SEM. P values were determined by one-way ANOVA with Tukey’s multiple comparisons test. ns, not significant. Source data are provided as a Source data file.