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Neutrophil Polarization Following Myocardial Infarction in Mice

Pro‐inflammatory N1 and anti‐inflammatory N2 neutrophil subtypes have recently been described in stroke. The objective of the current study was to investigate the temporal neutrophil polarization following myocardial infarction (MI) in mice and explore whether neutrophils show plasticity. Post‐MI, cardiac neutrophil infiltration peaked at day 1 and was returning to baseline levels by day 7. At day 1, isolated infarct neutrophils showed higher mRNA expression of pro‐inflammatory markers (Ccl3, Il‐1β, Il‐12a, and Tnf‐α) compared to day 0 neutrophils. By days 5 and 7 post‐MI, neutrophils displayed increased expression of anti‐inflammatory markers (Cd206 and Il‐10). Using flow cytometry, we found a gradual increase in Ly6G+CD206+ N2 neutrophils post‐MI, from 2.4±0.6% of total neutrophils at day 1 to 18.1±3.0% at day 7 post‐MI, consistent with the above data. To evaluate plasticity, peripheral blood neutrophils were isolated from mice without MI and stimulated with LPS+ IFN‐ɣ or IL‐4. LPS+ IFN‐ɣ significantly increased the expression of pro‐inflammatory markers (Ccl3, Ccl5, Il‐6, Il‐12a, and Tnf‐α), while IL‐4 upregulated the expression of anti‐inflammatory markers (Arg1, Cd206, Tgf‐β1, and Ym1), implying that neutrophils can be polarized to N1 by LPS+ IFN‐ɣ or to N2 by IL‐4. This study, for the first time, demonstrates that post‐MI cardiac neutrophils display distinct pro‐inflammatory and anti‐inflammatory phenotypes, and neutrophils show high plasticity in vitro.