Increased IL-1β, IL-8, and IL-17 mRNA Expression in Blood Mononuclear Cells Observed in a Prospective Ischemic Stroke Study

Abstract

Background and Purpose-Ischemic brain injury secondary to arterial occlusion is characterized by acute local inflammation, which involves accumulation of polymorphonuclear neutrophils (PMN). Factors that influence the recruitment of PMN could represent new therapeutic targets in acute stroke. In this prospective study we evaluated numbers of peripheral blood mononuclear cells (PBMC) expressing mRNA for interleukin (IL)-1␤, IL-8, and IL-17 and macrophage inflammatory protein-1␣ (MIP-1␣) after ischemic stroke. Methods-Peripheral blood was obtained on days 1 to 3, 4 to 10, and 20 to 31 after onset of symptoms. In situ hybridization with radiolabeled synthetic oligonucleotide probes was adopted to measure cytokine mRNA expression in PBMC. Plasma and cerebrospinal fluid levels of IL-8 were measured by an enzyme-linked immunosorbent assay. Results-Most

The etiology of poststroke depression: a review of the literature and a new hypothesis involving inflammatory cytokines

“…24,26,27 Patients with ischemic stroke were found to have increased levels of IL-1b 28 and elevated IL-1b mRNA in mononuclear cells. 29 Furthermore, studies of the IL-1 and IL-1RA genes suggest that polymorphisms in both IL-1a and IL-1RA genes may be associated with increased risk of stroke. [30][31][32] Similarly, TNF-a has been hypothesized to play an important role in neurodegeneration.…”

A Novel Cytokine Receptor-Ligand Pair

“…In vivo, its expression has been reported elevated in the rheumatoid synovium, in multiple sclerosis blood and cerebrospinal fluid, and in peripheral blood mononuclear cells following ischemic stroke (7)(8)(9)(10)(11). Is is also produced by tumorinfiltrating lymphocytes and increases tumorigenicity of human cervical tumors in nude mice (12,13).…”

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“…The IL-8 levels in the cerebrospinal fluid of patients with cerebral infarction increased significantly at the acute stage and were still higher than the controls at ninety days after cerebral infarction [14,15]. The IL-8 mRNA levels in peripheral blood mononuclear cells (PBMC) and the IL-8 concentrations in the plasma of patients with acute cerebral infarction have been shown to increase rapidly; additionally, these increased levels lasted 20 to 31 days after the stroke and were inversely correlated with neurologic impairment scores [14,[16][17][18]. Taken together, these findings demonstrate that IL-8 affects neurological recovery at the acute stage and the long-term outcome of patients after cerebral infarction.…”

“…It is well known that interleukin-1β (IL-1β) and tumor necrosis factor alpha (TNF-α) are strong stimulators of IL-8 expression. The expression of IL-1β mRNA by blood cells was decreased back to the normal level in 20 to 31 days after ischemic stroke [14]. The high level of TNF-α being released by blood cells can last more J Neurophysiol Neurol Disord 2014 | Vol 1: 203 than 90 days after stroke; however, this level of TNF-α does not have enough intensity to stimulate IL-8, presumably because it is inhibited by the anti platelet drugs given to patients during the therapy period [30][31][32].…”

“…Some animal studies revealed that an inhibitor of the IL-8 receptor, repertaxin, alleviated acute and long-term local inflammation and promoted long-term neurological recovery by reducing polymorphonuclear neutrophil infiltration to the ischemic focus after cerebral infarction [12,13]. The IL-8 levels in the cerebrospinal fluid of patients with cerebral infarction increased significantly at the acute stage and were still higher than the controls at ninety days after cerebral infarction [14,15]. The IL-8 mRNA levels in peripheral blood mononuclear cells (PBMC) and the IL-8 concentrations in the plasma of patients with acute cerebral infarction have been shown to increase rapidly; additionally, these increased levels lasted 20 to 31 days after the stroke and were inversely correlated with neurologic impairment scores [14,[16][17][18].…”