Serial measurements of levels of the chemokines CCL2, CCL3 and CCL5 in serum of patients with acute ischaemic stroke.

Inflammation, involving cytokine/chemokine expression, occurs after stroke and deteriorates its course with leukocyte-mediated brain infarct progression. Chemokines are cytokines attracting selective leukocyte subsets and subgrouping into the four major subfamilies, CC, CXC, C, and CX3C. The CC subfamily preferentially acts on mononuclears.

Interleukin-12 in acute ischemic stroke patients.

Cytokines are important mediators of stroke-induced immunological/inflammatory reaction which contributes to brain infarct progression as well as to the disease severity and outcome. The aim of the study was to evaluate the levels of the proinflammatory and immunomodulatory cytokine interleukin-12 (IL-12) in serum of acute ischemic stroke patients, and to investigate the relation between these levels and demographic, laboratory, neuroimaging, and clinical data. The study comprised 23 first-ever ischemic stroke patients and 15 age- and sex-matched controls.

CXCL1 (GRO-alpha) chemokine in acute ischaemic stroke patients.

The inflammation accompanies and exacerbates cerebral ischaemia. The infiltrated leucocytes are thought to contribute to tissue injury in stroke patients. GRO-alpha (CXCL1) is a potent neutrophil chemoattractant which may play an important role in pathophysiology of stroke.

Acute ischaemic stroke increases the erythrocyte sedimentation rate, which correlates with early brain damage.

The acute phase response follows tissue injury and contributes to its exacerbation with pro-inflammatory and pro-thrombotic mechanisms. Acute phase proteins promote erythrocyte aggregation and falling, with the result that the erythrocyte sedimentation rate (ESR) is a measure of the acute phase response. As the acute phase response accompanies ischaemic brain damage, we studied ESR values in patients within the first 24 hours of ischaemic stroke and evaluated whether these values may be related to the volume of anatomically relevant single hemispheric brain computed tomography (CT) areas observed at the same period, indicating early stroke-related cerebral changes.

Hyperthermia in ischemic stroke.

Hyperthermia following ischemic stroke is a common but undesirable event whose pathophysiology and clinical importance are not fully recognized. Hyperthermia in ischemic stroke may result from the brain infarct itself; however, the progress of biochemical and inflammatory mechanisms associated with cerebral ischemia is also relevant. Consequently, the presence of hyperthermia accentuates ischemic mechanisms within the penumbra, an area of reversibly impaired neuronal function surrounding the infarct, contributing to conversion of the penumbra into an irreversible lesion.

[Cytokines in clinical and experimental ischemic stroke].

Inflammatory reaction following acute cerebral ischaemia exacerbates infarct size and neurological deficit. Brain resident cells localised within ischaemic region rapidly synthesise cytokines, proteins involved in cellular communication. The cytokines become important mediators of endothelial-leukocyte interactions leading to the influx of haematogenous inflammatory cells into the brain ischaemic region.

IL-15 is elevated in sera of patients with relapsing-remitting multiple sclerosis.

Interleukin-15 is a novel cytokine produced by monocytes/macrophages and sharing several biological activities with IL-2. IL-15 induces T cell proliferation, enhances natural killer (NK) cell cytotoxicity and also stimulates B cells to proliferate and secrete immunoglobulins. The purpose of our study was to measure IL-15 levels in the serum and CSF of 21 patients with relapsing-remitting form of MS, 9 with active gadolinium enhancing lesions in MRI, 12 without enhancing MRI lesions and to compare the results with the control group.

Adhesion molecules of immunoglobulin gene superfamily in stroke.

Stroke-induced inflammatory reaction leads to the accumulation of leukocytes in the brain ischaemic region, where they exert a detrimental effect--promotion and extension of cerebral damage. Intracerebral infiltration of peripheral blood leukocytes requires prior endothelial-leukocyte interactions that are mediated by such cell surface proteins as adhesion molecules. Among adhesion molecules, it is the immunoglobulin gene superfamily (IgSF) that is responsible for strong attachment and transendothelial migration of leukocytes.