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. 2020 Nov 2;30(6):1208–1218. doi: 10.1111/bpa.12911

Table 1.

Contribution of myeloid cells to brain inflammation after ischemia in animal models and human stroke.

Cell type Animal studies Human studies
Neutrophils

  • Early infiltration (or accumulation in perivascular spaces) within the first days after ischemia (34, 52)

  • Release of proteases and reactive oxygen/nitrogen species (40, 100, 103)

  • Phagocytosis, anti‐inflammatory N2 neutrophils (22, 41)

  • Infiltration within the first week after stroke (18, 70), but no significant infiltration in another study (121)

  • MMP‐9 production causing blood–brain barrier breakdown and hemorrhagic transformation (46, 65, 101)

  • Neutrophil extracellular traps contribute to thrombus formation and failure of recanalization (30, 85)
Microglia

  • Activation and change of morphology within hours after ischemia (75, 81)

  • Loss in the ischemic core and accumulation in the penumbra (75, 81)

  • Production of reactive oxygen/nitrogen species, inflammatory cytokines, and chemokines (9, 51)

  • Phagocytosis, production of anti‐inflammatory cytokines, and growth factors (9, 51)

  • Loss in the ischemic core and proliferation in the penumbra within the first week after stroke (18, 70, 121)

  • Expression of pro‐inflammatory markers CD68, p22phox, CD86, CD163, and iNOS during resorption stage (121)

  • Production of TNFα (31)

  • Decreased expression of the homeostatic marker P2RY12 in acute lesions, the penumbra, and resorption stage (121)

  • Increased expression of the anti‐inflammatory marker CD206 in resorption phase (121)

  • Phagocytosis of tissue debris (121)
Monocytes/macrophages

  • Infiltration of CCR2+ inflammatory monocytes peaks around day 3 after ischemia (39)

  • Differentiation into CX3CR1+ macrophages (39)

  • CCR2+ monocytes mainly accumulate in lesion core surrounded by CX3CR1+ macrophages/monocytes (39)

  • Production of reactive oxygen/nitrogen species, pro‐inflammatory cytokines, and chemokines (51, 108)

  • Phagocytosis, promotion of vascular stability, and angiogenesis (43, 83)

  • Difficulties in distinguishing resident microglia from infiltrating monocytes/ macrophages

  • Substantial increase (especially in white matter lesions) of Iba1+TMEM119− cells suggests recruitment of peripheral monocytes to ischemic lesion (121)

  • Preferential accumulation around blood vessels in early lesions (121)

Table 1 summarizes key features of myeloid cell function after stroke, comparing data from animal models to results from human studies.