Proinflammatory cytokines: indicators of infection in high-risk patients

Faßbender, Klaus; Dempfle, Carl-Erik; Mielke, Orell; Rossol, S.; Schneider, Susanne A.; Dollman, M.; Hennerici, Michael G.

doi:10.1016/s0022-2143(97)90131-1

Cited by 34 publications

(29 citation statements)

References 22 publications

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“…However, we found sTNF-RI was increased at 5–7 d and the peak concentration in the first week correlated with infarct volume and outcome (mRS and BI) at 3 months and 1 year. This is consistent with earlier observations of elevated sTNF-RI concentration in stroke patients with nosocomial infection [26]. A more robust relationship between sTNF-RI and stroke severity or outcome may reflect a longer half-life of receptors compared to TNF-α.…”

Section: Discussionsupporting

confidence: 92%

Clinical outcome following acute ischaemic stroke relates to both activation and autoregulatory inhibition of cytokine production

et al. 2007

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Background: As critical mediators of local and systemic inflammatory responses, cytokines are produced in the brain following ischaemic stroke. Some have been detected in the circulation of stroke patients, but their role and source is unclear. Focusing primarily on interleukin(IL)-1-related mechanisms, we serially measured plasma inflammatory markers, and the production of cytokines by whole blood, from 36 patients recruited within 12 h and followed up to 1 year after acute ischaemic stroke (AIS).

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Section: Discussionsupporting

confidence: 92%

Clinical outcome following acute ischaemic stroke relates to both activation and autoregulatory inhibition of cytokine production

et al. 2007

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“…Increased expression of TNFR1 mRNA in the ipsilateral cortex was noted slightly during ischemia and was significantly increased at 12 h after reperfusion in tMCAO (Yin et al, 2004). A clinical study also showed that TNFR1 concentration increased in patients with acute ischemic stroke (Fassbender et al, 1997). By signaling through the Fasassociated death domain (FADD) and caspase-8, TNF-α may lead to apoptosis, whereas reacting with TNF-receptor associating factor 2 and receptor-interacting protein may lead to anti-inflammatory and anti-apoptotic functions (reviewed by (Hallenbeck, 2002).…”

Section: Cytokinesmentioning

confidence: 88%

The inflammatory response in stroke

Wang

Tang

Yenari

2007

Journal of Neuroimmunology

1,023

868

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Recent work in the area of stroke and brain ischemia has demonstrated the significance of the inflammatory response accompanying necrotic brain injury. Acutely, this response appears to contribute to ischemic pathology, and anti-inflammatory strategies have become popular. This chapter will discuss the current knowledge of the contribution of systemic and local inflammation in experimental stroke. It will review the role of specific cell types including leukocytes, endothelium, glia, microglia, the extracellular matrix and neurons. Intracellular inflammatory signaling pathways such as nuclear factor kappa beta and mitogen-activated protein kinases, and mediators produced by inflammatory cells such as cytokines, chemokines, reactive oxygen species and arachidonic acid metabolites will be reviewed as well as the potential for therapy in stroke and hypoxic-ischemic injury.

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“…Elevated IL-6 concentrations showed significant positive correlation with volume of computed tomography brain lesion as well as poor functional and neurologic outcome. There have been various other reports of elevated plasma IL-6 concentrations in patients who have had acute strokes (Beamer et al, 1995;Tarkowski et al, 1995;Kim et al, 1996;Fassbender et al, 1997;Carlstedt et al, 1997;Ferrarese et al, 1999;Vila et al, 2000a;Vila et al, 2000b). Stimulated blood cells from patients who have had a stroke show a significant increase in IL-6 release from days 1 to 2 until 1 month (Ferrarese et al, 1999).…”

Section: Molecular Components Of Inflammationmentioning

confidence: 99%

Inflammation and Infection in Clinical Stroke

Emsley

Tyrrell

2002

J Cereb Blood Flow Metab

202

126

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Summary:Stroke has enormous clinical, social, and economic implications, and demands a significant effort from both basic and clinical science in the search for successful therapies. Atherosclerosis, the pathologic process underlying most coronary artery disease and the majority of ischemic stroke in humans, is an inflammatory process. Complex interactions occur between the classic risk factors for atherosclerosis and its clinical consequences. These interactions appear to involve inflammatory mechanisms both in the periphery and in the CNS. Central nervous system inflammation is important in the pathophysiologic processes occurring after the onset of cerebral ischemia in ischemic stroke, subarachnoid hemorrhage, and head injury. In addition, inflammation in the CNS or in the periphery may be a risk factor for the initial development of cerebral ischemia. Peripheral infection and inflammatory processes are likely to be important in this respect. Thus, it appears that inflammation may be important both before, in predisposing to a stroke, and afterwards, where it is important in the mechanisms of cerebral injury and repair. Inflammation is mediated by both molecular components, including cytokines, and cellular components, such as leukocytes and microglia, many of which possess pro-and/or antiinflammatory properties, with harmful or beneficial effects. Classic acute-phase reactants and body temperature are also modified in stroke, and may be useful in the prediction of events, outcome, and as therapeutic targets. New imaging techniques are important clinically because they facilitate in vivo dynamic evaluation of tissue damage in relation to outcome. Inflammatory conditions such as giant cell arteritis and systemic lupus erythematosus predispose to stroke, as do a range of acute and chronic infections, principally respiratory. Diverse mechanisms have been proposed to account for inflammation and infection-associated stroke, ranging from classic risk factors to disturbances of the immune and coagulation systems. Considerable opportunities therefore exist for the development of novel therapies. It seems likely that drugs currently used in the treatment of stroke, such as aspirin, statins, and modulators of the renin-angiotensin-aldosterone system, act at least partly via antiinflammatory mechanisms. Newer approaches have included antimicrobial and antileukocyte strategies. One of the most promising avenues may be the use of cytokine antagonism, for example, interleukin-1 receptor antagonist.

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Proinflammatory cytokines: indicators of infection in high-risk patients

Cited by 34 publications

References 22 publications

Clinical outcome following acute ischaemic stroke relates to both activation and autoregulatory inhibition of cytokine production

Clinical outcome following acute ischaemic stroke relates to both activation and autoregulatory inhibition of cytokine production

The inflammatory response in stroke

Inflammation and Infection in Clinical Stroke

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