Fig. 3

S100A8/A9 blockade inhibits systemic inflammation but does not impact cardiac immune cell environment during endotoxemia. Endotoxemia was induced in C57Bl/6NrJ mice by intraperitoneal injection of 5 mg/kg LPS. The mice were treated with 30 mg/kg ABR-238901 or PBS intraperitoneally at 0 h and 6 h post-LPS. The mice were sacrificed at 24 h for plasma isolation and flow cytometric analysis (A, B, D, E), or at 12 h for cardiac gene expression (C). Cytokine levels were measured in plasma. A Heatmap of plasma cytokine changes following ABR-238901 treatment during endotoxemia, expressed as Z-score in relation to median. B Treatment effect on plasma levels of individual pro-inflammatory cytokines and chemokines. C Cardiac gene expression of NLRP3 inflammasome components, inflammatory cytokines, S100A8, S100A9 and BNP. D Gating strategy for flow cytometry analysis of cardiac CD45+ leukocytes. E Distribution of cardiac immune cell populations during endotoxemia, with and without S100A8/A9 blockade. Statistical differences between two groups were examined with Student’s t-test or Mann–Whitney test, following normality assessment with Shapiro–Wilk test. *P < 0.05, PBS, Phosphate Buffered Saline; ABR, ABR-238901; Eos, Eosinophils; NK, Natural Killer cells; Neu, Neutrophils; Monos, Monocytes; Mac, Macrophages; cDC, conventional dendritic cells. Data is represented as mean ± SD. A and B N = 5 per group, C N = 4-5 per group, D and E N = 5–8 per group