Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P05231 (interleukin-6)
 23,907 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pathophysiological mechanisms for vasospasm after subarachnoid haemorrhage (SAH) remain unclear and, so far, roles of cytokines in vasospasm have not been known. In the present study, we measured interleukin-1 alpha (IL-1 alpha), interleukin-1 beta (IL-1 beta), interleukin-6 (IL-6), interleukin-8 (IL-8), and tumour necrosis factor-alpha (TNF-alpha) concentrations in the cerebrospinal fluid (CSF) of patients with subarachnoid haemorrhage (SAH). ELISA assay were performed on 21 CSF samples from 7 patients with SAH and on 4 sera samples. Both IL-6 and IL-8 were detected in all CSF samples, but IL-1 alpha, IL-1 beta, and TNF-alpha were not detected. IL-6 and IL-8 were also detected in sera, but at much lower concentrations. This study indicates that IL-6 and IL-8 may play roles as immunomodulators in patients with SAH. In addition, it has been reported that IL-6 inhibits prostaglandin I2 production and increases the mRNA level of c-sis gene, suggesting that IL-6 may play an important role in vasospasm as vasoconstrictor.
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PMID:Cytokine production in cerebrospinal fluid after subarachnoid haemorrhage. 760 45

To investigate the influence of inducible nitric oxide synthase on cerebral arteries after subarachnoid haemorrhage (SAH) in vivo, lipopolysaccharide (LPS), a major inducer of inducible nitric oxide synthase, was injected intracisternally into control and SAH model dogs. Intracisternal injection of LPS (0.5 mg) produced a long-lasting, submaximal vasodilation of the basilar artery of control dogs on angiography. This effect became significant at 4 hours after LPS injection and plateaued after 6 hours. This vasodilation was reduced by N(G)-monomethyl-L-arginine. Vasopressin slightly suppressed the vasodilation, while bradykinin increased it. The concentration of L-arginine in CSF decreased after LPS injection, while that of L-citrulline increased. In cytokines, the concentration of tumour necrosis factor-alpha; (TNF-alpha;) in CSF increased transiently at 4 hours after LPS injection, while interleukin-1 beta, interleukin-6, interferon-gamma, did not change. These data suggest that vasodilation by LPS is mainly due to nitric oxide predominantly synthesized by an inducible nitric oxide synthase, proximally induced by TNF-alpha. Our data make it unlikely that SAH itself induces the inducible nitric oxide synthase in vascular tissue, since isolated endothelium-denuded basilar artery from SAH model dogs did not respond to L-arginine. In SAH model dogs, the degree of vasodilation by LPS differed with the severity of vasospasm. Vasodilation was much greater in mild than in severe vasospasm in dogs, and was increased by superoxide dismutase. These findings suggest that the induction of inducible nitric oxide synthase or its activity may be less effective in severe vasospasm.
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PMID:Vasodilation by intrathecal lipopolysaccharide of the cerebral arteries after subarachnoid haemorrhage in dogs. 886 3

The aim of the present study was to examine the changes of inflammatory and coagulation factors in blood of the internal jugular vein, not of peripheral vein, in patients with subarachnoid hemorrhage (SAH). The results show that while interleukin-6 (IL-6) and platelet activating factor (PAF) concentrations increased within first 4 days after SAH and remained elevated up to 14 days, interleukin-1 beta (IL-1 beta) showed a transient increase between 5-9 days after SAH and tumor necrosis factor-alpha (TNF-alpha) remained unchanged. Also different coagulation factors were increased between 5-9 days after SAH. Moreover, patients with delayed ischemic neurological deficits (DIND) displayed the highest levels of PAF and the coagulation factors, von Willebrand factor (vWF) and thrombin-antithrombin III complex (TAT). These results suggest that elevation of PAF and other inflammatory cytokines following SAH may cause the hypercoagulation state that is associated with cerebral vasospasm and internal jugular vein may be more adequate vessel for sampling blood to examine these factors.
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PMID:Elevation of platelet activating factor, inflammatory cytokines, and coagulation factors in the internal jugular vein of patients with subarachnoid hemorrhage. 934 29

The authors characterized the role of interleukins in the cerebrospinal fluid (CSF) in the development of vasospasm after subarachnoid haemorrhage (SAH), particularly interleukin-6 (IL-6). Concentrations of interleukin-1 beta (IL-1 beta), IL-6, and interleukin-8 (IL-8) were measured serially in CSF of 24 patients and in serum of 9 patients with SAH and correlated clinically. Additionally, the effects of the same cytokines on the cerebral arteries of dogs were analyzed on angiograms after intracisternal injection. Changes in levels of eicosanoids, angiogenic factors, and soluble cell adhesion molecules were investigated in the CSF of injected dogs. CSF concentrations of IL-6 and IL-8 were elevated significantly above control levels from the acute stage of SAH until the chronic stage. Patients with symptomatic vasospasm had significantly higher levels of IL-6 as well as IL-8 in CSF on days 5 and 7. Intracisternal injection of IL-6 induced long-lasting vasoconstriction in five out of eight dogs, while IL-8 did not. The diameter of canine basilar artery after IL-6 was reduced 29 +/- 5% from pretreatment diameter at 8 hours. Prostaglandins E2 and I2 were elevated in CSF for the first 4.5 hour of this IL-6-induced vasospasm. Neither angiogenic factors such as platelet-derived growth factor-AB and vascular endothelial growth factor nor soluble cell adhesion molecules were significantly elevated in CSF. IL-6, which increases to very high concentrations in CSF after SAH, may be important in inducing vasospasm, as IL-6 produced long-lasting vasoconstriction in the canine cerebral artery, which may be partly related to activation of the prostaglandin cascade.
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PMID:Interleukin-6 and development of vasospasm after subarachnoid haemorrhage. 984 32

Endothelial cell dysfunction may contribute to cerebral vasospasm and aggravation of ischemic brain damage following subarachnoid hemorrhage (SAH). It has been suggested that oxyhemoglobin derived from subarachnoid blood clots might be a prime candidate for cerebral vasospasm. In this study, cisternal bloody cerebrospinal fluid (bCSF) was collected from SAH patients four and seven days after aneurysmal rupture, and the effects of bCSF on the cell growth and intracellular calcium ion ([Ca2+]i) dynamics were investigated in cultured human umbilical vein endothelial cells. CSF collected from patients undergoing other intracranial surgeries was used as a control. Pre-treatment with bCSF4 significantly facilitated cell proliferation and DNA synthesis in the cultured endothelial cells, and significantly enhanced histamine-induced [Ca2+]i increase, while acute treatment of the bCSF elicited no [Ca2+]i change. Pre-treatment with interleukin-1 beta showed a similar significant enhancement of the histamine-induced [Ca2+]i response, while pre-treatment with high concentrations of serum or interleukin-6 did not change the [Ca2+]i response. It is concluded that bCSF collected from SAH patients contains some substances which enhance endothelial cell proliferation and sensitivity to inflammatory mediator.
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PMID:Bloody cerebrospinal fluid from patients with subarachnoid hemorrhage alters intracellular calcium regulation in cultured human vascular endothelial cells. 1104 21

Having demonstrated a transcranial gradient of the cytokine interleukin-6 (IL-6) in patients with either traumatic brain injury or spontaneous subarachnoid haemorrhage we have employed in situ hybridisation for IL-6 messenger RNA (mRNA) to determine the site of this IL-6 production within the central nervous system (CNS). A rodent weight drop model of traumatic brain injury was used. IL-6 mRNA levels in brains were determined 6 h after injury. Sham animals had normal constitutive expression for IL6 mRNA. In traumatised animals an intense area of IL-6 mRNA labelling was found below the hippocampus. Cells strongly expressing IL-6 mRNA were also seen in the dentate gyrus. This inflammatory cytokine is clearly implicated in the response to CNS injury, but whether this response is neuroprotective or pathological is uncertain.
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PMID:Expression of interleukin-6 messenger RNA in a rat model of diffuse axonal injury. 1245 28

We report the clinical and autopsy findings of a 71-year-old Japanese woman with rheumatoid meningitis. This patient developed subacute meningitis during an inactive stage of rheumatoid arthritis (RA), and despite intensive examinations no causative agents or underlying disease could be identified except for RA. Based on persistent hypocomplementaemia and increased serum levels of immune complexes she was suspected of having vasculitis, and was treated with intravenous methylprednisolone (1000 mg/day for 3 days) followed by oral prednisolone. Soon after beginning treatment with corticosteroid her symptoms improved, in parallel with a decrease in cell counts and interleukin-6 in the cerebrospinal fluid. During tapering of oral prednisolone she died of a subarachnoid haemorrhage which was ascribed to a relapse of the meningitis. Autopsy demonstrated infiltration of mononuclear cells, including plasma cells, in the leptomeninges, mainly around small vessels, leading to a definite diagnosis of rheumatoid meningitis. When RA patients manifest intractable meningitis with a subacute course, this disease is important as a possible diagnosis even if the arthritis is inactive, and intensive treatment, including corticosteroid and immunosuppressants, should be positively considered as a therapeutic option as soon as possible because of the poor prognosis.
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PMID:Rheumatoid meningitis: an autopsy report and review of the literature. 1467 33

The Janus kinase-signal transducer and activator of transcription (JAK-STAT) is one of the most important signaling pathways transducing signals from the cell surface in response to cytokines. Subarachnoid hemorrhage (SAH) produces cytokines in the CSF. We investigated whether this signaling pathway is activated in the rat basilar artery after SAH by cytokines. In a rat single-hemorrhage model of SAH, basilar arteries and CSF were obtained until 7 days after SAH. The concentration of interleukin-6 (IL-6) in CSF was measured by ELISA. Western blot analysis with JAK1, phosphospecific-JAK1, STAT3, phosphospecific STAT3 at Tyr705 and Ser727, cyclooxygenase-2 (COX-2), and actin antibodies was performed in basilar artery. The expressions of STAT3, phosphospecific STAT3 at Tyr705 and Ser727, and COX-2 in basilar artery were examined by immunohistochemical studies. The concentration of IL-6 immediately increased after SAH and Western blot analysis revealed that JAK1 was phosphorylated within 2 h, accompanied by phosphorylation of STAT3 at Tyr705, extending to Ser727 at days 1-2. Immunohistochemistry revealed phosphorylation of STAT3 to occur in endothelial and smooth muscle cells of the basilar artery. In addition, intracisternal injection of IL-6 by itself significantly increased phosphorylation of STAT3 at Tyr705 and Ser727. Expression of COX-2 was also upregulated in endothelial cells of the basilar artery. These results indicate that SAH produces the proinflammatory cytokine IL-6 in the CSF, which activates the JAK-STAT signaling pathway in the basilar artery and induces transcription of immediate early genes.
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PMID:Activation of the JAK-STAT signaling pathway in the rat basilar artery after subarachnoid hemorrhage. 1641 12

Cardiac myxoma is a source of emboli to the vascular tree, especially to the central nervous system. Although it is rare, its early recognition is particularly important because of its unique clinical features of subsequently leading to intracerebral or subarachnoid hemorrhage, even brain metastases, and its potential for surgical cure. Missing the diagnosis may lead to devastating results, including stroke, even sudden death. A 40-year-old male with no other conventional vascular risk factors such as hypertension, diabetes or hyperlipidemia presented with right hemiplegia, global aphasia, vomiting, and fever. Infarction over the left middle cerebral artery was disclosed on magnetic resonance imaging study, and echocardiogram showed a huge mass, about 5cm in size, on the mitral valve which was histopathologically proved to be a cardiac myxoma. He also presented with multiple emboli to the kidneys and the left eye. There is uncertainty about the role of anticoagulation. The treatment of choice remains surgical excision of the cardiac myxoma which may lead to normalization of serum interleukin-6 levels and resolution of constitutional symptoms, and the intracranial aneurysms may regress and resolve.
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PMID:Young stroke, cardiac myxoma, and multiple emboli: a case report and literature review. 1699 1

Rapid diagnosis and management of stroke patients is becoming increasingly important with the emergence of new interventional strategies for acute cerebral ischemia. A biochemical surrogate of cerebral ischemia, rapidly detectable in the serum before radiological diagnosis, might have clinical utility in the setting of acute stroke, high-risk cardiovascular procedures, and subarachnoid hemorrhage. Such a marker might also aid in the neurological prognosis of anoxic brain injury. Several serum markers have been evaluated in acute cerebral ischemia. These include neuronal enzymes such as neuron-specific enolase; markers of glial injury and activation, such as protein S100beta; and mediators of inflammation, such as interleukin-6. The clinical and preclinical data supporting the use of these biochemical surrogates of cerebral ischemia are reviewed.
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PMID:Serum markers of cerebral ischemia. 1789 90


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