Abstract: Post-ischemic inflammation is a coordinated process, which lasts from hours to days and involves recruitment of inflammatory cells from blood to the brain endothelial cells. Recently, the adhesion of leukocytes at endothelium, especially neutrophils, and its implication in post-stroke neuronal injury have been extensively explored and reported in both experimental and clinical  settings (Jian et al., 2019). However its role in diabetic patients following stroke is still elusive. Some significant differences such as risk factors, stroke subtypes and clinical outcomes are different between diabetic and non-diabetic. The higher prevalence of lacunar stroke, higher frequency of hypertension and lower neurological deficit at admission were reported earlier in diabetic patients. We found that early increase of neutrophils plays a prominent role in instigating a larger stroke size and worse clinical outcomes as compared to patients that do not have diabetes. After ischemic stroke, neutrophils are recruited to ischemic brain and can enter into the brain following hypoxia-ischemia (HI) through cerebral vessels, choroid plexus, and subarachnoid space. Figure 1A shows the various routes of entry of neutrophils in the db/db mouse brain 24 hours post stroke. Among all  immune cells, neutrophils  are  the first one to appear in the brain at day 1 post HI and remain until 7 days in the perilesional space, and subsequently other cells such as T & B lymphocytes  migrate to the lesion (Chu et al., 2014). These neutrophils remain in the vessel, release matrix metalloproteases and other proteases to damage the blood-brain barrier and the secondary damage starts, when neutrophils penetrate the brain parenchyma (Jickling et al., 2015) Previously, we have seen an increased matrix metalloproteinase-9 with graded infarct size and a direct relationship between matrix metalloproteinase-9 and neutrophils, which confirms the role of neutrophils mediating stroke injury (Kumari et al., 2020).