Elevation of Neutrophil CEACAM1 Associated with Multiple Inflammatory Mediators was Related to Different Disease Progression in Ischemic Stroke Patients

Abstract Background Tissue damage, expecially blood-brain barrier (BBB) injury caused by inflammatory factor storm and stroke-associated infection (SAI) during cerebral stroke is an important factor affecting the prognosis of patients. We aim to analyze the level of carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1) together with the multiple inflammatory mediators at different stages of ischemic stroke (IS), as well as to investigate the role of CEACAM1 and the potential underlying mechanism in IS in the meanwhile. Methods The frequency of CEACAM1 positive neutrophils, neutrophil viability and levels of intracellular cytokines were detected by flow cytometry. The plasma CEACAM1, neutrophil gelatinase-associated lipocalin (NGAL), matrix metalloproteinases-9 (MMP-9), interleukin-10 (IL-10) and tumor necrosis factor (TNF) were measured by ELISA. Results Compared with the normal control, the percentage of CEACAM1 positive neutrophils in the peripheral blood in the IS patients showed significant elevation, and a significant increase was also noticed in the content of plasma CEACAM1 at the subacute stage. There was a positive correlation between CEACAM1 expression rate in the neutrophils and plasma CEACAM1 and IL-10 content in the subacute group. Compared with the acute group and healthy control group, there was an instinct elevation in the level of plasma MMP-9 in the subacute group. The plasma NGAL in the subacute and stable groups was significantly higher than that of the normal control. Conclusion Our data showed that there was rapid elevation of CEACAM1 in the neutrophils at the acute stage of cerebral IS. We speculated that CEACAM1 may serve as an inhibitory regulator involved in the progression of focal cerebral ischemia. Moreover, the elevation of serum NGAL at the acute and stable stages may involve in the BBB injury mediated by MMP-9.