Increased expression of adhesion molecule CD18 (LFA-1β) on the leukocytes of peripheral blood in patients with acute ischemic stroke

Fiszer, Urszula; Korczak-Kowalska, G; Palasik, Witold; Korlak, J; Górski, Andrzej; Członkowska, Anna

doi:10.1111/j.1600-0404.1998.tb00641.x

Cited by 36 publications

(9 citation statements)

References 23 publications

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“…There is little pathology data on leukocyte-endothelial adhesion molecules in human ischemic stroke [13]. There is also little useful implication for the measurement of these molecules in clinical practice [15].…”

Section: Discussionmentioning

confidence: 99%

The value of leukocyte adhesion molecules in patients after ischemic stroke

et al. 2009

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Leukocyte recruitment and inflammatory response play an important patho-physiologic role after cerebral ischemia. This study aimed to evaluate whether leukocyte adhesion molecules can predict clinical outcome in patients after ischemic stroke. We prospectively examined serial changes in p-selectin glycoprotein ligand-1 (PSGL-1), macrophage antigen-1 (Mac-1), and lymphocyte function-associated antigen-1 (LFA-1) expression by leukocyte subsets using flow cytometry at various time points in 65 acute ischemic stroke patients and 60 controls. PSGL-1 expression on neutrophils and monocytes was significantly higher from day 1 to 90 after stroke as compared with control subjects (p < 0.05). The expression of monocyte Mac-1, LFA-1, and neutrophil Mac-1 were also significantly increased on days 1 and 7 after stroke than in control subjects (p < 0.05). Neutrophil PSGL-1 expression on day 1 was significantly higher in patients with early neurologic deterioration (END) (p < 0.01). Monocyte Mac-1 expression positively correlated with National Institutes of Health Stroke Scale (NIHSS) scores on admission (p = 0.013, gamma = 0.318). Underlying disease of diabetes mellitus and NIHSS score on admission were independently associated with 3-month outcome. The expressions of leukocyte adhesion molecules on admission are significantly increased in patients with acute ischemic stroke. This study shows that higher neutrophil PSGL-1 expression on admission may imply a higher risk for END and that monocyte Mac-1 expression on admission reflects the severity of ischemic stroke on admission.

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Section: Discussionmentioning

confidence: 99%

The value of leukocyte adhesion molecules in patients after ischemic stroke

et al. 2009

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“…The results of this study confirm the findings from other animal models that systemic neutrophil activation is important in cerebral reperfusion injury. Similar measures of neutrophil activation may be useful indicators of reperfusion injury in humans with ischemic stroke but to date have not been thoroughly investigated (Caimi et al, 2001; Fiszer et al, 1998; Tsai et al, 2009). The systemic neutrophil activation described in this study has additional significance in that transgenic mouse models bred on a C57Bl/6 background are increasingly used to elucidate single mechanisms of reperfusion injury after ischemic stroke.…”

Section: Discussionmentioning

confidence: 99%

Systemic Neutrophil Activation in a Mouse Model of Ischemic Stroke and Reperfusion

Morrison

McKee

Ritter

2010

Biological Research For Nursing

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As a natural response to injury and disease, neutrophils activate, adhere to the microvasculature, migrate into brain tissue, and release toxic substances such as reactive oxygen species and proteases. This neutrophil response occurs when blood flow is returned to brain tissue (reperfusion) after ischemic stroke. Thus, the presence of activated systemic neutrophils increases the potential for tissue injury during reperfusion after ischemic stroke. Although experiments in rat models suggest that activated neutrophils play a pivotal role in cerebral ischemia reperfusion injury, little is known about systemic neutrophil activation during reperfusion following ischemic stroke in a mouse model. The purpose of this study was to characterize systemic leukocyte responses and neutrophil CD11b expression 15-min and 24-hr post-reperfusion in a mouse model of ischemic stroke. The intraluminal filament method of transient middle cerebral artery occlusion (tMCAO) with reperfusion or a sham procedure was performed in male C57Bl/6 mice. Automated leukocyte counts and manual white blood cell (WBC) differential counts were measured. Flow cytometry was used to assess systemic neutrophil surface CD11b expression. The data suggest that the damaging potential of systemic neutrophil activation begins as early as 15 min and remains evident at 24 hr after the initiation of reperfusion. In addition, because transgenic mouse models, bred on a C57Bl/6 background, are increasingly used to elucidate single mechanisms of reperfusion injury after ischemic stroke, findings from this study are foundational for future investigations examining the damaging potential of neutrophil responses post-reperfusion after ischemic stroke in genetically altered mouse models within this background strain.

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“…Several lines of evidence indicate that the expression of intercellular adhesion molecule-1 (ICAM-1) (Stanimirovic et al, 1997;Yang et al, 1999;Yilmaz and Granger, 2010), P-selectin, E-selectin (Zhang et al, 1998;Huang et al, 2000), and integrins (Kim et al, 1995a;Fiszer et al, 1998) on endothelial cells can promote the adhesion and trans-endothelial migration of leukocytes (Okada et al, 1994;Lindsberg et al, 1996), thereby contributing to neuroinflammation-mediated neuronal cell death. In the ischemic brain, the expression of specific adhesion glycoproteins on cerebral microvascular endothelial cells was significantly increased following an ischemic insult.…”

Section: How Does the Injured Brain Activate The Immune System?mentioning

confidence: 99%

Molecular dialogs between the ischemic brain and the peripheral immune system: Dualistic roles in injury and repair

Chen

Shi

et al. 2014

Progress in Neurobiology

171

144

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Immune and inflammatory responses actively modulate the pathophysiological processes of acute brain injuries such as stroke. Soon after the onset of stroke, signals such as brain-derived antigens, danger-associated molecular patterns (DAMPs), cytokines, and chemokines are released from the injured brain into the systemic circulation. The injured brain also communicates with peripheral organs through the parasympathetic and sympathetic branches of the autonomic nervous system. Many of these diverse signals not only activate resident immune cells in the brain, but also trigger robust immune responses in the periphery. Peripheral immune cells then migrate toward the site of injury and release additional cytokines, chemokines, and other molecules, causing further disruptive or protective effects in the ischemic brain. Bidirectional communication between the injured brain and the peripheral immune system is now known to regulate the progression of stroke pathology as well as tissue repair. In the end, this exquisitely coordinated crosstalk helps determine the fate of animals after stroke. This article reviews the literature on ischemic brain-derived signals through which peripheral immune responses are triggered, and the potential impact of these peripheral responses on brain injury and repair. Pharmacological strategies and cell-based therapies that target the dialogue between the brain and peripheral immune system show promise as potential novel treatments for stroke.

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Increased expression of adhesion molecule CD18 (LFA-1β) on the leukocytes of peripheral blood in patients with acute ischemic stroke

Cited by 36 publications

References 23 publications

The value of leukocyte adhesion molecules in patients after ischemic stroke

The value of leukocyte adhesion molecules in patients after ischemic stroke

Systemic Neutrophil Activation in a Mouse Model of Ischemic Stroke and Reperfusion

Molecular dialogs between the ischemic brain and the peripheral immune system: Dualistic roles in injury and repair

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