Elevated levels of interleukin-6 may occur in cerebrospinal fluid from patients with recent epileptic seizures

Peltola, Jukka; Hurme, Mikko; Miettinen, A; Keränen, Tapani

doi:10.1016/s0920-1211(98)00024-2

Cited by 104 publications

(77 citation statements)

References 9 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Rapid induction of IL-6 expression in the brain is known to occur in most (if not all) neuropathological conditions, including seizures in humans (Lehtimäki et al, 2003(Lehtimäki et al, , 2004Peltola et al, 1998Peltola et al, , 2002Jankowsky and Patterson, 1999) where IL-6 levels in the cerebrospinal fluid up to 100 pg/ml have been found (Peltola et al, 2000). Astrocytes are a major source of IL-6 in the brain (van Wagoner and Benveniste, 1999).…”

Section: Discussionmentioning

confidence: 99%

“…It is known that the expression of A 1 receptors in WT mice is increased after neuropathological events, such as seizures Vanore et al, 2001;Angelatou et al, 1991Angelatou et al, , 1993. On the other hand, several reports have shown that those noxious conditions trigger the release of IL-6 (Lehtimäki et al, 2003;Peltola et al, 1998Peltola et al, , 2002. Accordingly, we used WT animals and IL-6-deficient mice to evaluate the relationship between the expression of IL-6 and the upregulation of adenosine A 1 receptors in response to PTZ-induced seizures.…”

Section: Influence Of Il-6 On Adenosine a 1 Receptors In Vivomentioning

confidence: 99%

See 1 more Smart Citation

Interleukin-6 Upregulates Neuronal Adenosine A1 Receptors: Implications for Neuromodulation and Neuroprotection

Biber

Pinto-Duarte

Wittendorp

et al. 2007

Neuropsychopharmacol

View full text Add to dashboard Cite

The immunological response in the brain is crucial to overcome neuropathological events. Some inflammatory mediators, such as the immunoregulatory cytokine interleukin-6 (IL-6) affect neuromodulation and may also play protective roles against various noxious conditions. However, the fundamental mechanisms underlying the long-term effects of IL-6 in the brain remain unclear. We now report that IL-6 increases the expression and function of the neuronal adenosine A 1 receptor, with relevant consequences to synaptic transmission and neuroprotection. IL-6-induced amplification of A 1 receptor function enhances the responses to readily released adenosine during hypoxia, enables neuronal rescue from glutamate-induced death, and protects animals from chemically induced convulsing seizures. Taken together, these results suggest that IL-6 minimizes the consequences of excitotoxic episodes on brain function through the enhancement of endogenous adenosinergic signaling.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Influence Of Il-6 On Adenosine a 1 Receptors In Vivomentioning

confidence: 99%

Interleukin-6 Upregulates Neuronal Adenosine A1 Receptors: Implications for Neuromodulation and Neuroprotection

Biber

Pinto-Duarte

Wittendorp

et al. 2007

Neuropsychopharmacol

View full text Add to dashboard Cite

show abstract

“…A considerable body of experimental and clinical evidence suggests that IL-1β, IL-6, and TNF-α are induced by seizure activity and that these cytokines contribute to the formation of structural changes, such as neuronal damage and gliosis, after sustained seizure activity (49)(50)(51). Interestingly, in patients with recent generalized tonic-clonic seizures, the IL-6 level was selectively elevated in cerebrospinal fluid (CSF) and plasma without any change in IL-1β and TNF-α levels (52), and the elevated plasma IL-6 level was correlated with peripheral blood leukocyte counts and CRP (53). Several studies have shown that the IL-6 level in the CSF is elevated in neuropsychiatric SLE (NPSLE) patients (54)(55)(56).…”

Section: Discussionmentioning

confidence: 99%

High-Sensitivity C-Reactive Protein as an Associate of Clinical Subsets and Organ Damage in Systemic Lupus Erythematosus

Lee

Singh

Link

et al. 2008

Seminars in Arthritis and Rheumatism

View full text Add to dashboard Cite

Objective-C-reactive protein (CRP) may play an anti-inflammatory role during the acute phase of inflammation, and is also used as a marker of inflammation associated with cardiovascular disease. In the present study, we investigated the association between high-sensitivity CRP (hsCRP) and systemic lupus erythematosus (SLE) manifestations, autoantibodies, and organ damage.Methods-In this cross-sectional study, 610 SLE patients from a prospective cohort had more than one hsCRP measurement. Organ damage was assessed using the Systemic Lupus International Collaborating Clinics (SLICC)/American College of Rheumatology (ACR) Damage Index. Multiple linear regression models were used to adjust for age, gender, ethnicity, disease duration, body mass index, education, disease activity, current prednisone dose, statin use, and estrogen use.Results-After adjusting for confounders, hsCRP was associated with myocarditis, cardiac murmur, interstitial pulmonary fibrosis, pulmonary hypertension, gastrointestinal lupus manifestations, and anemia. Anti-dsDNA antibodies and lupus anticoagulant were associated with hsCRP in unadjusted models, and these associations remained significant after adjustment for confounders. hsCRP levels were significantly higher in patients with pulmonary, musculoskeletal, and endocrine damage, and a total SLICC Damage Index score ≥1. After adjustment, hsCRP was associated with pulmonary, musculoskeletal, and total damage, but no longer with endocrine damage.Conclusions-hsCRP is associated with a broad range of clinical features and organ damage in SLE, particularly in the pulmonary and musculoskeletal systems. This association holds true independent of sociodemographic, disease activity, and treatment factors, and may be useful to identify high-risk SLE patients who would benefit from additional screening and surveillance studies.

show abstract

“…Importantly, there is evidence that NO and other inflammatory mediators increase as a result of ongoing seizure activity (Kaneko et al, 2002). Increased interleukin-6 (IL-6) protein levels have been observed in the CSF of epileptic patients (Peltola et al, 1998). Also, temporal lobe tissue from epileptic patients exhibits increased IL-1␤ immunoreactivity (Sheng et al, 1994).…”

Section: )mentioning

confidence: 99%

c-Jun N-Terminal Kinase Activation Responses Induced by Hippocampal Kindling Are Mediated by Reactive Astrocytes

Cole-Edwards¹,

Musto²,

Bazán³

2006

J. Neurosci.

View full text Add to dashboard Cite

Hippocampal kindling, a model of mesial temporal lobe epilepsy, is developed through repetitive stimulation of the hippocampus and leads to increased after-discharges as measured by EEG and an enduring seizure-prone state. Synthesis of new proteins is thought to form the basis for sustained seizure-induced physiological and/or pathological changes in synaptic reorganization and apoptotic/necrotic neuronal death. Here we examined the effect of kindling on stimulus-induced c-Jun N-terminal kinase (JNK) and p38 phosphorylation, events postulated to lie upstream of seizure-induced changes in gene transcription. We found that stimulus-induced phosphorylation of JNK, but not of p38, is significantly enhanced in kindled animals compared with their naive counterparts in the CA1 subregion of the hippocampus. Immunofluorescent staining confirmed this region-specific pattern of JNK activation and revealed that reactive astrocytes mediate this effect. Astrocyte proliferation and hypertrophy, as well as upregulation of vimentin protein levels, common markers of astrogliosis, were present after 4 d of kindling. Moreover, this reactive astrogliosis was associated with neuronal death as visualized with Fluoro-jade B and anti-active caspase-3 staining. Stimulus-induced phosphorylation of the JNK substrate paxillin was enhanced in kindled animals, but not that of c-Jun. Moreover, a pan-antibody against MAPK/CDK (mitogen-activated protein kinases/cyclindependent kinase) substrates indicated the presence of phosphorylated proteins in cytosolic, membrane, and nuclear fractions. The consequence of these phosphorylation events is not completely understood, but these findings suggest a selective astrocytic signaling response to aberrant synaptic activity, signaling that may modulate kindling progression and/or neuronal death.

show abstract

Elevated levels of interleukin-6 may occur in cerebrospinal fluid from patients with recent epileptic seizures

Cited by 104 publications

References 9 publications

Interleukin-6 Upregulates Neuronal Adenosine A1 Receptors: Implications for Neuromodulation and Neuroprotection

Interleukin-6 Upregulates Neuronal Adenosine A1 Receptors: Implications for Neuromodulation and Neuroprotection

High-Sensitivity C-Reactive Protein as an Associate of Clinical Subsets and Organ Damage in Systemic Lupus Erythematosus

c-Jun N-Terminal Kinase Activation Responses Induced by Hippocampal Kindling Are Mediated by Reactive Astrocytes

Contact Info

Product

Resources

About