Early Intrathecal Production of Interleukin-6 Predicts the Size of Brain Lesion in Stroke

Tarkowski, E; Rosengren, Lars; Blomstrand, Christian; Wikkelsø, Carsten; Jensen, Christer; Ekholm, Sven; Tarkowski, Andrzej

doi:10.1161/01.str.26.8.1393

Cited by 341 publications

(273 citation statements)

References 32 publications

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“…In contrast, the IL-1RA has neuroprotective effects in both rodents and humans. 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.…”

Section: Resultsmentioning

confidence: 99%

“…[38][39][40] Although a clear picture of the role of IL-6 in stroke has not yet been elucidated, an increase in IL-6 production following cerebral ischemia has been described in several clinical studies 21,34,41,42 and elevated levels of the IL-6 cytokine have been correlated with severity and clinical outcome of stroke. 28,43,44 Furthermore, polymorphisms of the promoter IL-6 gene have been associated with stroke 45,46 and the IL-6 system has been associated with acute inflammatory response after stroke. 47 In addition, the IL-8 chemokine has also been associated with the recruitment of inflammatory cells and is increased in stroke patients.…”

Section: Resultsmentioning

confidence: 99%

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

et al. 2006

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Although poststroke depression is unlikely to represent a single disorder and numerous etiologies for different kinds of poststroke depression will likely emerge as the result of future research, we believe that a number of poststroke depressive disorders are likely to be the result of specific changes in brain pathology and neurophysiology. Nevertheless, there are relatively few hypotheses about the pathophysiology of poststroke depression. This paper, therefore, proposes a new hypothesis for poststroke depression involving increased production of proinflammatory cytokines resulting from brain ischemia in cerebral areas linked to the pathogenesis of mood disorders. This paper reviews the evidence supporting the hypothesis that proinflammatory cytokines are involved in the occurrence of stroke as well as mood disorders linked to the brain damage. The increased production of proinflammatory cytokines such as IL-1b, TNF-a or IL-18 resulting from stroke may lead to an amplification of the inflammatory process, particularly in limbic areas, and widespread activation of indoleamine 2,3-dioxygenase (IDO) and subsequently to depletion of serotonin in paralimbic regions such as the ventral lateral frontal cortex, polar temporal cortex and basal ganglia. The resultant physiological dysfunction may lead to poststroke depression. Future investigations may explore this hypothesis through more extensive studies on the role of proinflammatory cytokines, such as IL-1b, TNF-a or even IL-18, in patients with poststroke depression. Molecular Psychiatry (2006) 11, 984-991.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

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

et al. 2006

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“…Association with infarct area Parallel with CRP, FNG, and IL-1ra Tarkowski et al (1995) 30 1-90 days…”

Section: Serum Interleukin-6 In Stroke Patientsmentioning

confidence: 96%

Ambivalent Aspects of Interleukin-6 in Cerebral Ischemia: Inflammatory versus Neurotrophic Aspects

Suzuki

Tanaka

Suzuki

2008

J Cereb Blood Flow Metab

217

177

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Interleukin-6 (IL-6) is pleiotropic cytokine involved in many central nervous system disorders including stroke, and elevated serum IL-6 has been found in acute stroke patients. IL-6 is implicated in the inflammation, which contributes to both injury and repair process after cerebral ischemia. However, IL-6 is one of the neurotrophic cytokines sharing a common receptor subunit, gp130, with other neurotrophic cytokines, such as leukemia inhibitory factor (LIF) and ciliary neurotrophic factor. The expression of IL-6 is most prominently identified in neurons in the peri-ischemic regions, and LIF expression shows a similar pattern. The direct injection of these cytokines into the brain after ischemia can reduce ischemic brain injury. The cytokine receptors are localized on the neuron surface, suggesting that neurons are the cytokine target. The major IL-6 downstream signaling pathway is JAK-STAT, and Stat3 activation occurs mainly in neurons during postischemic reperfusion. Further investigation is necessary to clarify the exact role of Stat3 signaling in neuroprotection. Taken together, the information suggests that IL-6 plays a double role in cerebral ischemia, as an inflammatory mediator during the acute phase and as a neurotrophic mediator between the subacute and prolonged phases.

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“…There was only weak reactivity with IL-4 [23]. Addition of anti-IL-6 antibody reduced proliferative response of B9 cells to IL-6 by at least 95% [25].…”

Section: Serological Analysismentioning

confidence: 94%

Inhibition of nitric oxide synthase (NOS) aggravates Staphylococcus aureus septicaemia and septic arthritis

Sakiniene

Bremell

Tarkowski

1997

Clinical and Experimental Immunology

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SUMMARYThe aim of this study was to assess the role of NO and its metabolites in bacterial arthritis. The murine model of haematogenously acquired septic arthritis was used. Swiss mice treated with NOS inhibitors (N G -monomethyl-L-arginine or N q -nitro-L-arginine methyl ester) were injected intravenously with toxic shock syndrome toxin-1 (TSST-1) producing Staphylococcus aureus LS-1. Arthritis was evaluated clinically and histopathologically. Serum cytokine levels, bacterial isolates and intracellular capacity of macrophages to kill bacteria were also analysed. The frequency of arthritis in mice treated with NOS inhibitors was three to four-fold higher than that in non-treated controls (75% versus 20%). The severity of arthritis, expressed as mean arthritic index, was 1 . 4 and 0 . 4, respectively. Cartilage and/or bone destruction occurred in 63% of NOS inhibitor-treated mice, but only in 10% of controls. Also, the cumulative septicaemia-induced mortality was clearly higher in mice treated with NOS inhibitors compared with non-treated controls. Intracellular killing capacity of the peritoneal macrophages, treated in vitro with NOS inhibitors, was decreased. Thus, 24 h after bacterial inoculation peritoneal macrophages pretreated with NOS inhibitors killed more than 10 times less bacteria than the control ones (P < 0 . 01). We conclude that NOS inhibitors aggravate S. aureus arthritis, possibly by inducing impairment of the intracellular killing capacity of macrophages.

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Early Intrathecal Production of Interleukin-6 Predicts the Size of Brain Lesion in Stroke

Cited by 341 publications

References 32 publications

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

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

Ambivalent Aspects of Interleukin-6 in Cerebral Ischemia: Inflammatory versus Neurotrophic Aspects

Inhibition of nitric oxide synthase (NOS) aggravates Staphylococcus aureus septicaemia and septic arthritis

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