MoDMs in rMCAO March 2026

All of the data that has been acquired so far in our project investigating the role of blood-borne macrophages in neurologic repair after delayed recanaliton in a rodent permanent MCAO stroke model. We hypothesize that blood-borne monocytes/macrophages which populate the infarction core and penumbra after delayed recanalization adopt an efferocytic and anti-inflammatory phenotype, driven by IL-13/4, aiding in repair and recovery after pMCAO in rats. Preliminary data supports that hypothesis with animals undergoing delayed recanalization (rMCAO) having decreased infarction volume and slightly increased neurological functioning. Immunofluorescence also shows colocalization of CD163 with CD44 in rMCAO indicating blood borne macrophages are adopting an anti-inflammatory phenotype after delayed recanaluization while there is more colocalization of CD86 with CD44 in permanently occluded animals (pMCAO) indicating blood borne macrophages adopting a pro-inflammatory phenotype when animals do not receive restored blood flow.