This PDF file includes:

• Fig. S1. Subclinical endotoxin up-regulates MPO level in HFD-fed mice.
• Fig. S2. Subclinical endotoxemia exacerbates atherosclerotic pathogenesis in RD-fed mice.
• Fig. S3. Subclinical endotoxin causes neutrophil expansion in atherosclerotic mice.
• Fig. S4. Subclinical endotoxin primes neutrophils into a proinflammatory state in atherosclerotic mice.
• Fig. S5. Subclinical endotoxin induces oxCAMKII elevation in vivo.
• Fig. S6. Neutrophils maintain viability after in vitro polarization.
• Fig. S7. Transfusion of superlow-dose LPS–polarized neutrophils elevates plasma lipid levels and modulates lesional macrophages.
• Fig. S8. Superlow-dose LPS and oxLDL treatment elevates ROS accumulation in neutrophils.
• Fig. S9. 4-PBA reverses superlow-dose LPS–induced differential regulation of miR-24 and miR-126 in neutrophils.
• Fig. S10. Transfusion of 4-PBA–polarized neutrophils down-regulates plasma lipid levels and reduces lesional macrophage activation.

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