scholarly journals 9. Elevated TNF-α Levels in Cerebrospinal Fluid of Patients With Schizophrenia

2017 ◽  
Vol 43 (suppl_1) ◽  
pp. S10-S10
Author(s):  
Juan Gallego ◽  
Christopher Morell ◽  
Robert McNamara ◽  
Todd Lencz ◽  
Anil Malhotra
Keyword(s):  
Cerebrospinal Fluid ◽  
Tnf Α

scholarly journals Inhibition of Leukocyte Entry into the Brain by the Selectin Blocker Fucoidin Decreases Interleukin-1 (IL-1) Levels but Increases IL-8 Levels in Cerebrospinal Fluid during Experimental Pneumococcal Meningitis in Rabbits

2000 ◽  
Vol 68 (6) ◽  
pp. 3153-3157 ◽  
Author(s):  
Christian Østergaard ◽  
Runa Vavia Yieng-Kow ◽  
Thomas Benfield ◽  
Niels Frimodt-Møller ◽  
Frank Espersen ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Pneumococcal Meningitis ◽  
Interleukin 1 ◽  
Treated Group ◽  
Control Group ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Significant Difference ◽  
The Brain ◽  
Experimental Pneumococcal Meningitis

ABSTRACT The polysaccharide fucoidin is a selectin blocker that inhibits leukocyte recruitment into the cerebrospinal fluid (CSF) during experimental pneumococcal meningitis. In the present study, the effect of fucoidin treatment on the release of the proinflammatory cytokines tumor necrosis factor alpha (TNF-α), interleukin-1 (IL-1), and IL-8 into the CSF was investigated. Rabbits (n = 7) were treated intravenously with 10 mg of fucoidin/kg of body weight every second hour starting 4 h after intracisternal inoculation of ∼106 CFU of Streptococcus pneumoniae type 3 (untreated control group, n = 7). CSF samples were obtained every second hour during a 16-h study period. Treatment with fucoidin caused a consistent and significant decrease in CSF IL-1 levels (in picograms per milliliter) between 12 and 16 h (0 versus 170, 0 versus 526, and 60 versus 1,467, respectively;P < 0.02). A less consistent decrease in CSF TNF-α levels was observed in the fucoidin-treated group, but with no significant difference between the two groups (P > 0.05). In contrast, there was no attenuation in CSF IL-8 levels. Indeed, there was a significant increase in CSF IL-8 levels (in picograms per milliliter) in the fucoidin-treated group at 10 and 12 h (921 versus 574 and 1,397 versus 569, respectively;P < 0.09). In conclusion, our results suggest that blood-derived leukocytes mainly are responsible for the release of IL-1 and to some degree TNF-α into the CSF during pneumococcal meningitis, whereas IL-8 may be produced by local cells within the brain.

scholarly journals Cerebral Malaria in Children: Serum and Cerebrospinal Fluid TNF‐α and TGF‐β Levels and Their Relationship to Clinical Outcome

2003 ◽  
Vol 49 (4) ◽  
pp. 216-223 ◽  
Author(s):  
Fabian Esamai ◽  
Jan Ernerudh ◽  
Helena Janols ◽  
Susanne Welin ◽  
Christina Ekerfelt ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Clinical Outcome ◽  
Cerebral Malaria ◽  
Tnf Α

Cerebrospinal fluid of chronic osteoarthritic patients induced interleukin-6 release in human glial cell-line T98G

2020 ◽  
Author(s):  
Weiling Liu ◽  
Chunmei Li ◽  
Francis Chee Kuan Tan ◽  
Hong Jye Neo ◽  
Yiong Huak Chan ◽  
...  
Keyword(s):  
Chronic Pain ◽  
Cerebrospinal Fluid ◽  
Cell Line ◽  
Pain Score ◽  
Western Blotting ◽  
Interleukin 6 ◽  
Antibody Array ◽  
T98g Cell ◽  
Cell Lysate ◽  
Tnf Α

Abstract Background Chronic osteoarthritic pain is not well understood in terms of its pathophysiological mechanism. Activated glial cells are thought to play a role in the maintenance of chronic pain. T98G glioblastoma cell line was previously observed to release higher amounts of interleukin-6 (IL-6) when treated with cerebrospinal fluid (CSF) from patients with another chronic pain condition, post-herpetic neuralgia. In this study, we investigated the ability of CSF from patients diagnosed with knee osteoarthritis suffering from chronic pain, to trigger the release of pro-inflammatory cytokines, IL-6, IL-1beta and tumour necrosis factor alpha (TNF-α) from T98G. Characterization of upstream signalling was also explored. Methods 15 osteoarthritis patients undergoing total knee replacement due to chronic knee pain and 15 patients without pain undergoing other surgeries with spinal anaesthesia were prospectively recruited. CSF was collected during anaesthesia. CSF were added to cultured T98G cells in the presence of lipopolysaccharide. IL-6, IL-1β and TNF-α release from T98G cells were measured using enzyme immunoassay. Antibody array and western blotting were performed using CSF-triggered T98G cell lysates to identify possible signalling targets. Age, gender and pain scores were recorded. Mann-Whitney U test was used to compare IL-6 release and protein expression between groups. Association between IL-6 and pain score was analysed using linear regression. Results Significant higher levels of IL-6 were released by T98G cells when induced by osteoarthritis patients' CSF in presence of lipopolysaccharide. IL-6 levels showed positive association with pain score (adjusted B estimate= 10.1 (95% Confidence Interval 4.3-15.9); p= 0.001). Antibody array conducted with 6 pooled T98G cell lysate induced with osteoarthritis pain patient CSF identified greater than 2-fold proteins including STE20-related kinase adaptor protein and spleen tyrosine kinase. Further validation done using western blotting of individual CSF-triggered T98G cell lysate showed non-significant increase. Conclusion Higher IL-6 release from T98G when triggered by OA CSF, in the presence of lipopolysaccharide, suggest presence of "unknown molecule" in CSF that may be crucial in the maintenance phase of chronic pain in our osteoarthritis population. Further studies on the signalling pathways involved in pain and relevance of IL-6 release from T98G in other pain models are needed.

Brain-blood permeability: TNF-α promotes escape of protein tracer from CSF to blood

2000 ◽  
Vol 279 (1) ◽  
pp. R148-R151 ◽  
Author(s):  
Jodi B. Dickstein ◽  
Harvey Moldofsky ◽  
John B. Hay
Keyword(s):  
Central Nervous System ◽  
Cerebrospinal Fluid ◽  
Nervous System ◽  
Tumor Necrosis ◽  
Venous Blood ◽  
Protein Clearance ◽  
Tracer Recovery ◽  
Tnf Α ◽  
The Central Nervous System ◽  
Necrosis Factor

The objective of this study was to determine the effect of tumor necrosis factor (TNF)-α on the efflux of protein from the central nervous system to blood based on assessing the clearance of radiolabeled albumin from the cerebrospinal fluid (CSF) to blood in rats. 125I-labeled human serum albumin (125I-HSA) was injected into a lateral ventricle, and venous blood was sampled hourly to determine the basal CSF protein clearance into the blood. After this, rats were intraventricularly infused with 10 μl TNF-α and 10 μl131I-HSA ( n = 6) or 10 μl saline and 10 μl 131I-HSA ( n = 6). Venous blood was sampled hourly for 3 h. 131I-HSA tracer recovery increased threefold in the venous blood and was significantly higher in the spleen, muscles, and skin in animals treated with TNF-α. No significant changes were observed in control animals treated with saline. The data suggest that TNF-α promotes the clearance of protein macromolecules from the CSF to the venous blood.

Cerebrospinal fluid IL-6, HSP72, and TNF-α in exercising humans

2006 ◽  
Vol 20 (6) ◽  
pp. 585-589 ◽  
Author(s):  
Adam Steensberg ◽  
Mads K. Dalsgaard ◽  
Niels H. Secher ◽  
Bente Klarlund Pedersen
Keyword(s):  
Cerebrospinal Fluid ◽  
Tnf Α

Cortisol is increased in postmortem cerebrospinal fluid of multiple sclerosis patients: relationship with cytokines and sepsis

2002 ◽  
Vol 8 (3) ◽  
pp. 229-236 ◽  
Author(s):  
Z A Erkut ◽  
E Endert ◽  
I Huitinga ◽  
D F Swaab
Keyword(s):  
Multiple Sclerosis ◽  
Cerebrospinal Fluid ◽  
Hpa Axis ◽  
Complex Interactions ◽  
Tnf Α ◽  
Cytokine Levels ◽  
Stimulation Tests ◽  
Cortisol Levels ◽  
Highly Correlated ◽  
Multiple Sclerosis Patients

Hypothalamo-pituitary-adrenal (HPA) axis activity is altered in patients with multiple sclerosis (MS), resulting in elevated basal levels and enhanced response of cortisol in stimulation tests. HPA axis hyperactivation in MS is thought to be the result of complex interactions of genetic, immunologic, and neuroendocrinological mechanisms. In order to investigate whether cytokine levels in the central nervous system are associated with the activation of the HPA axis in MS, we measured cortisol, interleukin (IL)-6, IL-10 and TNF-α levels in postmortem cerebrospinal fluid (CSF) of 18 patients with severe MS and 50 controls. We also investigated the cortisol and cytokine levels in the CSF of a group of MS patients and controls who died with sepsis, in order to see whether acute infectious situations affect the association between cortisol and cytokines. The cortisol levels in MS patients were increased by 80% in comparison to controls (p =0.008). There was no difference in IL-6 levels between the groups, while IL-10 and TNF-α levels of the majority of subjects were below detection limits. There was a positive correlation between cortisol and IL-6 only in control patients with sepsis (r=0.89, p =0.019), but not within the MS patients with sepsis or MS and control groups without sepsis. Cortisol levels in postmortem serum and CSF were highly correlated (r >0.78, p <0.001). We concluded that the basal level of cortisol is significantly increased in the CSF of MS patients and that IL-6 is not responsible for this rise. The relationship between cortisol and IL-6 in sepsis is discussed.

scholarly journals Cerebrospinal fluid of chronic osteoarthritic patients induced interleukin-6 release in human glial cell-line T98G

2019 ◽  
Author(s):  
Weiling Liu ◽  
Chunmei Li ◽  
Francis Chee Kuan Tan ◽  
Hong Jye Neo ◽  
Yiong Huak Chan ◽  
...  
Keyword(s):  
Chronic Pain ◽  
Cerebrospinal Fluid ◽  
Cell Line ◽  
Pain Score ◽  
Western Blotting ◽  
Interleukin 6 ◽  
Adaptor Protein ◽  
Antibody Array ◽  
Post Herpetic Neuralgia ◽  
Tnf Α

Abstract Background: Chronic osteoarthritic pain is not well understood in terms of its pathophysiological mechanism. Activated glial cells are thought to play a role in the maintenance of chronic pain. T98G glioblastoma cell line was previously observed to release higher amounts of interleukin-6 (IL-6) when treated with cerebrospinal fluid (CSF) from patients with another chronic pain condition, post-herpetic neuralgia. In this study, we investigated the ability of CSF from patients diagnosed with knee osteoarthritis (OA) suffering from chronic pain, to trigger the release of pro-inflammatory cytokines, IL-6, IL-1beta and tumour necrosis factor alpha (TNF-α) from T98G. Characterization of upstream signalling was also explored. Methods: 15 OA patients undergoing total knee replacement and 15 patients without pain undergoing surgery with spinal anaesthesia were prospectively recruited. CSF was collected during anaesthesia prior to surgery. CSF were added to cultured T98G cells. IL-6, IL-1β and TNF-α release from T98G cells were measured using enzyme immunoassay. Antibody array and western blotting were performed on CSF-triggered T98G cell lysates to identify possible signalling targets. Age, gender and pain scores were recorded. Mann-Whitney U test was used to compare IL-6 release and protein expression between groups. Association between IL-6 and pain score was analysed using linear regression.Results: Compared to CSF of patients without pain, significantly higher IL-6 levels were released by T98G cells when induced by CSF from OA patients. The IL-6 levels showed positive association with pain score (adjusted B estimate= 10.1 (95% Confidence Interval 4.3-15.9); p= 0.001). Array conducted with OA pain patient pooled CSF identified several proteins being upregulated greater than 2-fold including STE20-related kinase adaptor protein and spleen tyrosine kinase. Further validation in western blotting of individual samples was unable to show similar significant increase.Conclusion: IL-6 is a potential biomarker crucial in the maintenance phase of chronic pain in both OA and post-herpetic neuralgia (PHN). Identification of signalling pathways involved in pain using pooled CSF on antibody array yield several protein of interest. However, those targets are inconsistent when individually validated using western blotting. Exploring other protein targets is required to identify the signalling mechanism of chronic pain.

Neopterin and Cytokines in Non-pleocytotic Cerebrospinal Fluid in Child Patients

Pteridines ◽  
2000 ◽  
Vol 11 (4) ◽  
pp. 142-146
Author(s):  
Yasuhiko Kawakami ◽  
Kentaro Kuwabara ◽  
Takehisa Fujita ◽  
Osamu Fujino ◽  
Yoshitaka Fukunaga
Keyword(s):  
Cerebrospinal Fluid ◽  
Immune Activation ◽  
Serum Levels ◽  
Microglial Cells ◽  
Febrile Convulsions ◽  
Exanthem Subitum ◽  
Tnf Α ◽  
Child Patients ◽  
Ifn Γ

Abstract CSF and serum levels of neopterin and several kinds of CSF cytokines were measured in child patients with non-pleocytotic CSF. The CSF neopterin levels with febrile convulsions (FCs) were 27.4±33.0 nmol/1 and the CSF neopterinlserum neopterin ratio (C/S ratio) with FCs was 2.07±2.06. The longer the FCs patients' convulsions lasted, the higher their CSF neopterin levels tended to be come. The CSF neopterin levels with FCs were significantly higher than in those with pyrexia without convulsions (6.5±2.5 nmol/L) or convulsions without pyrexia, including epilepsy (4.9±2.9 nmol/L). The C/S ratio was also higher in patients with FCs than in those with pyrexia without convulsions (0.31±0.17) or convulsions without pyrexia (0.82±0.50).In addition, there was a tendency for CSF IFN-γ levels to be higher in patients with FCs than in those with pyrexia without convulsions or convulsions without pyrexia. However, TNF-α and IL-1α were under measurable levels in cases of non-pi eocytotic CSF. The CSF neopterin levels in patients with exanthem subitum with FCs were higher than in those without FCs. It has been reported that there is a possibility of neopterin production by microglial cells. Our finding that CSF neopterin levels were elevated in patients with FCs, whose CSF had no pleocytosis, are consistent with the possibility of neopterin production by microglia. Our results further suggest that immune activation of microgrial cells is one of the mechanisms involved in the onset of FCs.

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