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

Abstract Objective Aim of this study is to evaluate the effect of craniospinal interventions on cerebrospinal fluid (CSF) flow hydrodynamics and study the correlation of postoperative changes in flow alteration with clinical outcome. Materials and Methods Fifty patients who underwent various craniospinal procedures were studied using conventional and phase-contrast magnetic resonance imaging (PCMRI) protocol. CSF flow quantification was performed at cerebral aqueduct, foramen magnum, C2–3, and D12–L1 vertebral levels with site showing maximal alteration of CSF flow dynamics considered as the region of interest. Velocity encoding was kept at 20 cm/s. Patients with pathology atcraniovertebral junction were considered separately (group I) from others (group II) due to different flow dynamics. Follow-up scans were performed after an interval of 1 month for temporal evaluation of changes in CSF flow dynamics. Results Patients in both groups showed a significant change in peak CSF velocity postoperatively (mean change of 1.34 cm/s in group I and 0.28 cm/s in group II) with bidirectional improvement in flow on cine-phase-contrast qualitative images. Regional pain (82%) and headache (46%) were seen in most of the patients preoperatively. Postoperatively clinical symptoms improved in 59.5%, static in 26.2%, and worsened in 14.3%. In both the groups, an improvement in clinical symptomatology had significant correlation with mean changes in peak CSF velocity postoperatively (p = 0.04 in both groups). Conclusion PCMRI can effectively evaluate changes in CSF flow noninvasively both pre- and postoperatively. This may have potential role in determining clinical outcome and prognosis of patients undergoing procedures in craniospinal axis.

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

Schizophrenia Bulletin ◽

10.1093/schbul/sbx021.028 ◽

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

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Metabolites from cerebrospinal fluid in aneurysmal subarachnoid haemorrhage correlate with vasospasm and clinical outcome: a pattern-recognition1H NMR study

NMR in Biomedicine ◽

10.1002/nbm.918 ◽

2005 ◽

Vol 18 (1) ◽

pp. 24-33 ◽

Cited By ~ 49

Author(s):

Victoria G. Dunne ◽

Shermina Bhattachayya ◽

Michael Besser ◽

Caroline Rae ◽

Julian L. Griffin

Keyword(s):

Cerebrospinal Fluid ◽

Clinical Outcome ◽

Subarachnoid Haemorrhage ◽

Aneurysmal Subarachnoid Haemorrhage ◽

Nmr Study

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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

Infection and Immunity ◽

10.1128/iai.68.6.3153-3157.2000 ◽

2000 ◽

Vol 68 (6) ◽

pp. 3153-3157 ◽

Cited By ~ 47

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.

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Quantifying Enlargement of Brain Cerebrospinal Fluid Spaces: A Differential Equation Approach to Clinical Outcome in Melancholia

Neurology Psychiatry and Brain Research ◽

10.1016/j.npbr.2020.10.005 ◽

2020 ◽

Vol 38 ◽

pp. 92-96

Author(s):

Anisha Das

Keyword(s):

Differential Equation ◽

Cerebrospinal Fluid ◽

Clinical Outcome ◽

Equation Approach

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Correlation of tumor necrosis factor levels in the serum and cerebrospinal fluid with clinical outcome in Japanese encephalitis patients

Journal of Medical Virology ◽

10.1002/(sici)1096-9071(199702)51:2<132::aid-jmv8>3.0.co;2-8 ◽

1997 ◽

Vol 51 (2) ◽

pp. 132-136 ◽

Cited By ~ 81

Author(s):

V. Ravi ◽

Shreemanta Parida ◽

Anita Desai ◽

A. Chandramuki ◽

M. Gourie-Devi ◽

...

Keyword(s):

Cerebrospinal Fluid ◽

Tumor Necrosis Factor ◽

Clinical Outcome ◽

Japanese Encephalitis ◽

Tumor Necrosis ◽

Necrosis Factor

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

10.21203/rs.2.15747/v2 ◽

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.

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