Increased Cytokine Release from Peripheral Blood Cells after Acute Stroke

Ferrarese, Carlo; Mascarucci, Paolo; Zoia, Chiara Paola; Cavarretta, Rosella; Frigo, M.; Begni, Barbara; Sarinella, Federica; Frattola, L.; Simoni, M.G. De

doi:10.1097/00004647-199909000-00008

Cited by 188 publications

(146 citation statements)

References 40 publications

Supporting

Mentioning

131

Contrasting

Unclassified

Order By: Relevance

“…33 TNF-a release from blood cells and serum levels of TNF-a were found to be elevated during the acute phase following stroke compared with healthy controls. [34][35][36] Furthermore, increased levels of TNF-a in the cerebral spinal fluid and serum of acute stroke patients has been associated with increased severity of postischemic neuropathology 37 and polymorphism of the TNF gene have been associated with susceptibility to ischemic stroke. 32 IL-6 is a pleiotropic cytokine involved in inflammatory processes and like IL-1 is able to induce acute inflammatory responses such as fibrinogen and C-reactive protein production.…”

Section: Resultsmentioning

confidence: 99%

“…The C-reactive protein, an important peripheral inflammatory marker, is strongly associated with risk for stroke. [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.…”

Section: Resultsmentioning

confidence: 99%

See 1 more Smart Citation

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

et al. 2006

View full text Add to dashboard Cite

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.

show abstract

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

View full text Add to dashboard Cite

show abstract

“…Knowledge of the molecules participating in this pathogenic cascade causing neuronal damage probably represents a chance to recognize possible serum markers of ischemic stroke useful to a diagnostic algorithm of acute ischemic stroke. Increases of the proinflammatory cytokines interleukin-1␤, IL-6 and TNF-␣ have been detected in the ischemic cortex 1 h after middle cerebral artery (MCA) occlusion in experimental models of brain ischemia [8], and several studies have reported elevations of these proinflammatory cytokines in peripheral blood as well as in cerebrospinal fluid in patients with ischemic stroke [15][16][17][18][19][20]. Nevertheless, pathogenesis of brain ischemia involves both immuno-inflammatory and thrombotic mechanisms, so a good diagnostic panel for ischemic stroke should include a representative biomarker of both these pathogenic aspects.…”

Section: Discussionmentioning

confidence: 99%

Immuno-inflammatory and thrombotic/fibrinolytic variables associated with acute ischemic stroke diagnosis

et al. 2009

View full text Add to dashboard Cite

a b s t r a c tIntroduction: Accumulating evidence suggests that inflammation plays an important role in the development of acute cerebrovascular disease. The aim of this study is to evaluate the predictive value of a series of candidate serum immuno-inflammatory and thrombotic/fibrinolitic molecules towards diagnosis of acute ischemic stroke. Materials and methods:We enrolled 120 consecutive patients with a diagnosis of acute ischemic stroke and 123 consecutive hospitalized control patients without a diagnosis of acute ischemic stroke. We evaluated plasma levels of IL-1␤, TNF-␤, IL-6 and IL-10, E-selectin, P-selectin, sICAM-1 and sVCAM-1 as markers of immuno-inflammatory activation, vWF plasma levels as a marker of endothelial dysfunction, TPA antigen and PAI-1 plasma levels as a marker of a prothrombotic state. Results: TNF-␣, PAI-1 and TPA on bivariate logistic regression were highly correlated to stroke diagnosis. Among the other variables maintained in the final model IL␤, Selectin E, were significantly associated with acute ischemic stroke diagnosis, whereas IL-6, VICAM-1, ICAM-1 and neutrophil percentage showed only a slight or no association with stroke diagnosis. Furthermore, only the continuous values of TNF-␣, PAI-1 and TPA showed a significant predictive value and likelihood ratio, with an area under the ROC curve of 98.6%, 97.1% and 99.9%, respectively. Discussion: Our findings could suggest the high diagnostic power of these immuno-inflammatory and thrombotic/fibrinolytic variables in patients with acute ischemic stroke. Although our results are encouraging, additional studies are needed to establish the validity of this approach.

show abstract

“…Parallel with IL-1a Higher level in CSF IL-6 (231 ± 313 pg/ml) Ferrarese et al (1999) 40 (20) 1-90 days…”

Section: Serum Interleukin-6 In Stroke Patientsmentioning

confidence: 99%

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

Suzuki

Tanaka

Suzuki

2008

J Cereb Blood Flow Metab

220

177

View full text Add to dashboard Cite

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.

show abstract

Increased Cytokine Release from Peripheral Blood Cells after Acute Stroke

Cited by 188 publications

References 40 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

Immuno-inflammatory and thrombotic/fibrinolytic variables associated with acute ischemic stroke diagnosis

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

Contact Info

Product

Resources

About