ICAM-1 expression on human brain microvascular endothelial cells

Hess, David C.; Bhutwala, Tiku; Sheppard, James C.; Zhao, Wei; Smith, Joseph G.

doi:10.1016/0304-3940(94)90450-2

Cited by 71 publications

(33 citation statements)

References 8 publications

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“…Adhesion molecules involved in leukocyte adhesion and migration belong either to the selectin family such as P-selectin and E-selectin or to the immunoglobulin superfamily, such as intercellular adhesion molecule-1 (ICAM-1) or vascular cell adhesion molecule-1 (VCAM-1). These molecules are either present on BMEC in a resting state or can be expressed or further upregulated following stimulation by different proinflammatory factors (Brayton et al, 1998;Defazio et al, 1998;Dufour et al, 1998;Hess et al, 1994). Elevated levels of soluble ICAM-1 in cerebrospinal fluid of the patients with HIV-associated neurological diseases confirm the significance of upregulation of adhesion molecules in the pathogenesis of this disease (Heidenreich et al, 1994).…”

Section: Hiv-1 Entry Into the Cns: The Role Of Brain Endothelial Cellmentioning

confidence: 77%

Mechanisms of the Blood–Brain Barrier Disruption in HIV-1 Infection

et al. 2005

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(1) Alterations of brain microvasculature and the disruption of the blood-brain barrier (BBB) integrity are commonly associated with human immunodeficiency virus type 1 (HIV-1) infection. These changes are most frequently found in human immunodeficiency virus-related encephalitis (HIVE) and in human immunodeficiency virus-associated dementia (HAD). (2) It has been hypothesized that the disruption of the BBB occurs early in the course of HIV-1 infection and can be responsible for HIV-1 entry into the CNS. (3) The current review discusses the mechanisms of injury to brain endothelial cells and alterations of the BBB integrity in HIV-infection with focus on the vascular effects of HIV Tat protein. In addition, this review describes the mechanisms of the BBB disruption due to HIV-1 or Tat protein interaction with selected risk factors for HIV infection, such as substance abuse and aging.

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Section: Hiv-1 Entry Into the Cns: The Role Of Brain Endothelial Cellmentioning

confidence: 77%

Mechanisms of the Blood–Brain Barrier Disruption in HIV-1 Infection

et al. 2005

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“…Adhesion molecules are also expressed by human brain microvascular endothelium. The expression of ICAM-1, VCAM-1, and E-selectin by cerebral microvascular endothelial cells is increased by IL-1␤, TNF-␣, lipopolysaccharide (Hess et al, 1994;Stanimirovic et al, 1997), and in vitro ischemia-like insults (Stanimirovic et al, 1997). Intercellular adhesion molecule-1 expression by brain microvessels is significantly increased in the cerebral infarcts of patients who die after ischemic stroke (Lindsberg et al, 1996).…”

Section: Molecular Components Of Inflammationmentioning

confidence: 99%

Inflammation and Infection in Clinical Stroke

Emsley

Tyrrell

2002

J Cereb Blood Flow Metab

202

126

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Summary:Stroke has enormous clinical, social, and economic implications, and demands a significant effort from both basic and clinical science in the search for successful therapies. Atherosclerosis, the pathologic process underlying most coronary artery disease and the majority of ischemic stroke in humans, is an inflammatory process. Complex interactions occur between the classic risk factors for atherosclerosis and its clinical consequences. These interactions appear to involve inflammatory mechanisms both in the periphery and in the CNS. Central nervous system inflammation is important in the pathophysiologic processes occurring after the onset of cerebral ischemia in ischemic stroke, subarachnoid hemorrhage, and head injury. In addition, inflammation in the CNS or in the periphery may be a risk factor for the initial development of cerebral ischemia. Peripheral infection and inflammatory processes are likely to be important in this respect. Thus, it appears that inflammation may be important both before, in predisposing to a stroke, and afterwards, where it is important in the mechanisms of cerebral injury and repair. Inflammation is mediated by both molecular components, including cytokines, and cellular components, such as leukocytes and microglia, many of which possess pro-and/or antiinflammatory properties, with harmful or beneficial effects. Classic acute-phase reactants and body temperature are also modified in stroke, and may be useful in the prediction of events, outcome, and as therapeutic targets. New imaging techniques are important clinically because they facilitate in vivo dynamic evaluation of tissue damage in relation to outcome. Inflammatory conditions such as giant cell arteritis and systemic lupus erythematosus predispose to stroke, as do a range of acute and chronic infections, principally respiratory. Diverse mechanisms have been proposed to account for inflammation and infection-associated stroke, ranging from classic risk factors to disturbances of the immune and coagulation systems. Considerable opportunities therefore exist for the development of novel therapies. It seems likely that drugs currently used in the treatment of stroke, such as aspirin, statins, and modulators of the renin-angiotensin-aldosterone system, act at least partly via antiinflammatory mechanisms. Newer approaches have included antimicrobial and antileukocyte strategies. One of the most promising avenues may be the use of cytokine antagonism, for example, interleukin-1 receptor antagonist.

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“…The adherence, migration and accumulation of leukocytes play an important role in mediating neuonal injury during acute cerebral ischemia, resulting in BBB disruption, increasing cerebral edema and plugging the cerebral microvasculature. Recent studies have shown that endothelial cell adhesion molecules, such as intercellular adhesion molecule-1 (ICAM-1), are required for the migration of leukocytes into the brain (Hess et al, 1994).…”

mentioning

confidence: 99%