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      Peak plasma interleukin-6 and other peripheral markers of inflammation in the first week of ischaemic stroke correlate with brain infarct volume, stroke severity and long-term outcome

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          Abstract

          Background

          Cerebral ischaemia initiates an inflammatory response in the brain and periphery. We assessed the relationship between peak values of plasma interleukin-6 (IL-6) in the first week after ischaemic stroke, with measures of stroke severity and outcome.

          Methods

          Thirty-seven patients with ischaemic stroke were prospectively recruited. Plasma IL-6, and other markers of peripheral inflammation, were measured at pre-determined timepoints in the first week after stroke onset. Primary analyses were the association between peak plasma IL-6 concentration with both modified Rankin score (mRS) at 3 months and computed tomography (CT) brain infarct volume.

          Results

          Peak plasma IL-6 concentration correlated significantly (p < 0.001) with CT brain infarct volume (r = 0.75) and mRS at 3 months (r = 0.72). It correlated similarly with clinical outcome at 12 months or stroke severity. Strong associations were also noted between either peak plasma C-reactive protein (CRP) concentration or white blood cell (WBC) count, and all outcome measures.

          Conclusions

          These data provide evidence that the magnitude of the peripheral inflammatory response is related to the severity of acute ischaemic stroke, and clinical outcome.

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          Most cited references41

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          Classification and natural history of clinically identifiable subtypes of cerebral infarction.

          J. Bamford, P Sandercock, M. Dennis … (1991)
          We describe the incidence and natural history of four clinically identifiable subgroups of cerebral infarction in a community-based study of 675 patients with first-ever stroke. Of 543 patients with a cerebral infarct, 92 (17%) had large anterior circulation infarcts with both cortical and subcortical involvement (total anterior circulation infarcts, TACI); 185 (34%) had more restricted and predominantly cortical infarcts (partial anterior circulation infarcts, PACI); 129 (24%) had infarcts clearly associated with the vertebrobasilar arterial territory (posterior circulation infarcts, POCI); and 137 (25%) had infarcts confined to the territory of the deep perforating arteries (lacunar infarcts, LACI). There were striking differences in natural history between the groups. The TACI group had a negligible chance of good functional outcome and mortality was high. More than twice as many deaths were due to the complications of immobility than to direct neurological sequelae of the infarct. Patients in the PACI group were much more likely to have an early recurrent stroke than were patients in other groups. Those in the POCI group were at greater risk of a recurrent stroke later in the first year after the index event but had the best chance of a good functional outcome. Despite the small anatomical size of the infarcts in the LACI group, many patients remained substantially handicapped. The findings have important implications for the planning of stroke treatment trials and suggest that various therapies could be directed specifically at the subgroups.
          Article 0 comments Cited 307 times – based on 0 reviews     Review now
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            Correlations and interactions in the production of interleukin-6 (IL-6), IL-1, and tumor necrosis factor (TNF) in human blood mononuclear cells: IL-6 suppresses IL-1 and TNF.

            S Endres, R Schindler, J Mancilla … (1990)
            Interleukin-6 (IL-6) shares several biologic properties with IL-1, including hematopoietin-1 activity and stimulation of T cells. Because many of their biologic activities overlap, we developed and used a specific radioimmunoassay (RIA) for IL-6 to compare production of this cytokine on a molar basis with that of IL-1 alpha, IL-1 beta, and tumor necrosis factor (TNF)alpha. The RIA correlated well with the hybridoma bioassay for IL-6 (r = .87, P less than .001). Freshly isolated human peripheral blood mononuclear cells (PBMC) cultured in the absence of stimuli did not produce IL-6 in most cases. Kinetics of secretion and cell-association of IL-6 were studied. In contrast to IL-1 alpha but similar to TNF, IL-6 was almost entirely secreted into the extracellular fluid. Incubation with different stimuli (lipopolysaccharide [LPS], phytohemagglutinin [PHA], Staphylococcus epidermidis, or IL-1 alpha) resulted in production of IL-6. However, on a molar basis PBMC produced approximately two to three times less IL-6 than IL-1 alpha, IL-1 beta, or TNF, regardless of the stimulus. The amount of IL-6 produced from PBMC was consistent when measured in the same subjects six time during a 12-week period. In a cohort of 38 donors, the coefficient of variation for IL-6 production was .32, compared with .92 for IL-1 beta and .96 for TNF. Comparing cytokine production by PBMC, there was a significant correlation between IL-6 and IL-1 beta (r = .72) and between IL-6 and TNF (r = .66). IL-6 did not stimulate IL-1 beta or TNF production, but suppressed IL-1 beta and TNF production induced by LPS or PHA by 30% (P less than .01). This suppression of IL-1 beta and TNF by IL-6 appears to be on the level of transcription.
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              Cytokines and the nervous system II: Actions and mechanisms of action.

              Nancy J Rothwell, Stephen J Hopkins (1995)
              Cytokines exert diverse actions on the PNS and the CNS and have been implicated in neuronally mediated responses to disease and injury. Certain cytokines participate in the central control of host systemic responses to disease, acting as signals to and within the brain. These molecules are also involved in neuronal degeneration and repair in the PNS and CNS, and have been proposed as mediators of various neuropathologies. The actions, mechanisms of action and potential strategies for modifying cytokines in the nervous system will be considered in this review, which continues the discussion of cytokine expression and recognition published in the February issue of TINS.
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                Author and article information

                Journal
                Journal ID (nlm-ta): BMC Neurol
                Title: BMC Neurology
                Publisher: BioMed Central (London )
                ISSN (Electronic): 1471-2377
                Publication date Collection: 2004
                Publication date (Electronic): 15 January 2004
                Volume: 4
                Page: 2
                Affiliations
                [1 ]University of Manchester, Manchester M13 9PT, UK
                [2 ]Stroke Services, Clinical Sciences Building, Hope Hospital, Salford, M6 8HD, UK
                [3 ]Accident and Emergency Medicine, Hope Hospital, Salford M6 8HD, UK
                [4 ]Biostatistics Group, University of Manchester, Hope Hospital, Salford M6 8HD, UK
                [5 ]Department of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, CA, USA
                [6 ]Stroke Branch, National Institute of Neurological Disorders and Stroke, NIH, Bethesda, MD, USA
                [7 ]School of Biological Sciences, University of Manchester, Manchester M13 9PT, UK
                [8 ]North Western Injury Research Collaboration (NWIRC), Clinical Sciences Building, Hope Hospital, Salford M6 8HD, UK
                Article
                Publisher ID: 1471-2377-4-2
                DOI: 10.1186/1471-2377-4-2
                PMC ID: 331413
                PubMed ID: 14725719
                SO-VID: fec31e7d-9121-4bcc-82a8-b595e11c1f49
                Copyright © Copyright © 2004 Smith et al; licensee BioMed Central Ltd. This is an Open Access article: verbatim copying and redistribution of this article are permitted in all media for any purpose, provided this notice is preserved along with the article's original URL.
                History
                Date received : 15 August 2003
                Date accepted : 15 January 2004
                Categories
                Subject: Research Article

                ScienceOpen disciplines: Neurology
                Keywords: stroke acute,c-reactive protein,outcome measures,inflammation,interleukin-6
                Data availability:
                ScienceOpen disciplines: Neurology
                Keywords: stroke acute, c-reactive protein, outcome measures, inflammation, interleukin-6

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