Elevation of neutrophil carcinoembryonic antigen‐related cell adhesion molecule 1 associated with multiple inflammatory mediators was related to different clinical stages in ischemic stroke patients

Abstract

Background: We aimed to analyze the level of carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1) in neutrophils of ischemic stroke (IS) patients at different stages, together with its roles in neutrophils.Patients and methods: Sixty-seven patients were classified into acute phase group (n = 19), subacute phase group (n = 28), and stable phase group (n = 20), and 20 healthy individuals who had received physical examination at the same time period as healthy control. We then analyzed the expression level of CEACAM1 and cell viability in CEACAM1 positive and CEACAM1 negative neutrophils by flow cytometry and the content of plasma CEACAM1, neutrophil gelatinase-associated lipocalin (NGAL), matrix metalloproteinases-9 (MMP-9) was measured using enzyme-linked immunosorbent assay (ELISA), while that of interleukin-10 (IL-10) and tumor necrosis factor (TNF) was determined using a Human Enhanced Sensitivity Flex set.Results: Compared with healthy control, the percentage of CEACAM1 positive neutrophils in IS patients showed a significant increase, and a significant increase was also noticed in the content of plasma CEACAM1 at the subacute stage. Reduction in cell viability was observed in CEACAM1 positive neutrophils compared with CEACAM1 negative counterparts. There was a positive correlation between CEACAM1 expression rate in neutrophils and plasma CEACAM1 and IL-10 content in the subacute group. Compared with acute group and healthy control group, there was an instinct increase in the level of plasma MMP-9 and NGAL in subacute group. Conclusions:Our data showed that there was a rapid increase of CEACAM1 in neutrophils at the acute stage of IS. We speculated that CEACAM1 may serve as an inhibitory regulator involving in the progression of IS.

Understanding COVID-19 progression with longitudinal peripheral blood mononuclear cell proteomics: Changes in the cellular proteome over time

“…Furthermore, the presence of LDNs in PBMCs may be associated with emergency hematopoiesis/granulopoiesis in these patients, 48 which is in agreement with the increase in the abundance of multiple inflammatory signals, such as IL-6, IL-8, IL-10, and G-CSF, which prolong the lifespan of neutrophils and infiltration 15 , 47 , 49 as well as high levels of neutrophil proliferation and degranulation marks 50 , 51 and leukocytes rolling mediators over vascular surfaces. 52 Additionally, the results of plasma biomarkers, particularly at D0 and D7, align with the state of inflammation and alterations of metabolic pathways observed in the proteome of PBMCs from these patients.…”

Higher serum lipocalin 2 is associated with post-stroke depression at discharge

“…When stroke occurs, reactive astrocytes, activated microglia, neurons, choroid plexus and endothelial cells synthesize and secrete LCN2 in response to inflammation or damage to the brain [ 34 ]. It is reported that elevated levels of LCN2 in human plasma 1–3 days after ischaemic stroke [ 35 , 36 ], and plasma LCN2 still has a high expression level in the subacute phase [ 37 ]. Significantly elevated LCN2 in cerebrospinal fluid (CSF) or peripheral blood is associated with poor functional prognosis after stroke [ 14 ].…”

“…Relevant basic studies have shown that after ischemic stroke, elevated LCN2 activates various inflammatory pathways in glial cells, leading to glial cell proliferation, cytokine production and enhanced inflammatory response, so that neuroinflammation persists [ 34 ]. The abnormal increase of LCN2 not only directly destroys the BBB, but also forms a complex with matrix metallopeptidase-9 (MMP-9), which prolongs the activity of MMP-9 and participates in the destruction of the BBB [ 37 ]. Moreover, peripheral neurotoxic substances that pass through the damaged BBB also exacerbate neuroinflammation.…”

Molecular Mechanisms of Inflammasome in Ischemic Stroke Pathogenesis

“…The first cells to be activated following Ischemic brain damage are those of microglia. Subsequently, the monocytes/macrophages and the neutrophils also reach the ischemic area passing the blood–brain barrier (BBB) interacting with the adhesion molecules [ 26 , 27 ]. During reperfusion, glial cells and neurons secrete chemo-attractant protein-1 monocyte (MCP-1/CCL2), which causes the migration of neutrophils into the infarcted area [ 28 ].…”