THE INFLUENCE OF THE PROINFLAMMATORY CYTOKINE, OSTEOPONTIN, ON AUTOIMMUNE DEMYELINATING DISEASE

2002 ◽  
Author(s):  
D. Chabas ◽  
S.E. Baranzini ◽  
D. Mitchell ◽  
C.C. Bernard ◽  
S.R. Rittling ◽  
...  
Keyword(s):  
Proinflammatory Cytokine ◽  
Demyelinating Disease

scholarly journals Transition from Acute to Persistent Theiler's Virus Infection Requires Active Viral Replication That Drives Proinflammatory Cytokine Expression and Chronic Demyelinating Disease

2004 ◽  
Vol 78 (22) ◽  
pp. 12480-12488 ◽  
Author(s):  
Mark Trottier ◽  
Brian P. Schlitt ◽  
Aisha Y. Kung ◽  
Howard L. Lipton
Keyword(s):  
Spinal Cord ◽  
Viral Replication ◽  
Proinflammatory Cytokine ◽  
Viral Genome ◽  
Demyelinating Disease ◽  
Rna Replication ◽  
Viral Rna ◽  
Mrna Levels ◽  
Active Viral Replication ◽  
The Brain

ABSTRACT The dynamics of Theiler's murine encephalomyelitis virus (TMEV) RNA replication in the central nervous systems of susceptible and resistant strains of mice were examined by quantitative real-time reverse transcription-PCR and were found to correlate with host immune responses. During the acute phase of infection in both susceptible and resistant mice, levels of viral replication were high in the brain and brain stem, while levels of viral genome equivalents were 10- to 100-fold lower in the spinal cord. In the brain, viral RNA replication decreased after a peak at 5 days postinfection (p.i.), in parallel with the appearance of virus-specific antibody responses; however, by 15 days p.i., viral RNA levels began to increase in the spinal cords of susceptible mice. During the transition to and the persistent phase of infection, the numbers of viral genome equivalents in the spinal cord varied substantially for individual mice, but high levels were consistently associated with high levels of proinflammatory Th1 cytokine and chemokine mRNAs. Moreover, a large number of viral genome equivalents and high proinflammatory cytokine mRNA levels in spinal cords were only observed for susceptible SJL/J mice who developed demyelinating disease. These results suggest that TMEV persistence requires active viral replication beginning about day 11 p.i. and that active viral replication with high viral genome loads leads to increased levels of Th1 cytokines that drive disease progression in infected mice.

scholarly journals Infection with Theiler's Murine Encephalomyelitis Virus Directly Induces Proinflammatory Cytokines in Primary Astrocytes via NF-κB Activation: Potential Role for the Initiation of Demyelinating Disease

2003 ◽  
Vol 77 (11) ◽  
pp. 6322-6331 ◽  
Author(s):  
JoAnn P. Palma ◽  
Daeho Kwon ◽  
Neil A. Clipstone ◽  
Byung S. Kim
Keyword(s):  
Proinflammatory Cytokine ◽  
Demyelinating Disease ◽  
Cytokine Gene Expression ◽  
Cytokine Gene ◽  
Theiler's Murine Encephalomyelitis Virus ◽  
Cytokine Genes ◽  
Theiler’S Murine Encephalomyelitis Virus ◽  
Cytokine Activation ◽  
Immune Mediated ◽  
Encephalomyelitis Virus

ABSTRACT Theiler's virus infection in the central nervous system (CNS) induces a demyelinating disease very similar to human multiple sclerosis. We have assessed cytokine gene activation upon Theiler's murine encephalomyelitis virus (TMEV) infection and potential mechanisms in order to delineate the early events in viral infection that lead to immune-mediated demyelinating disease. Infection of SJL/J primary astrocyte cultures induces selective proinflammatory cytokine genes (interleukin-12p40 [IL-12p40], IL-1, IL-6, tumor necrosis factor alpha, and beta interferon [IFN-β]) important in the innate immune response to infection. We find that TMEV-induced cytokine gene expression is mediated by the NF-κB pathway based on the early nuclear NF-κB translocation and suppression of cytokine activation in the presence of specific inhibitors of the NF-κB pathway. Further studies show this to be partly independent of dsRNA-dependent protein kinase (PKR) and IFN-α/β pathways. Altogether, these results demonstrate that infection of astrocytes and other CNS-resident cells by TMEV provides the early NF-κB-mediated signals that directly activate various proinflammatory cytokine genes involved in the initiation and amplification of inflammatory responses in the CNS known to be critical for the development of immune-mediated demyelination.

Therapeutic Plasma Exchange Application in Children Requires Individual Decision

2020 ◽  
Author(s):  
Gürkan Atay ◽  
Demet Demirkol
Keyword(s):  
Plasma Exchange ◽  
Vascular Access ◽  
Pediatric Patients ◽  
Demyelinating Disease ◽  
Pediatric Intensive Care ◽  
Therapeutic Plasma Exchange ◽  
Transplantation Rejection ◽  
Access Problems ◽  
Uremic Syndrome

AbstractTherapeutic plasma exchange (TPE) is a treatment administered with the aim of removing a pathogenic material or compound causing morbidity in a variety of neurologic, hematologic, renal, and autoimmune diseases. In this study, we aimed to assess the indications, efficacy, reliability, complications, and treatment response of pediatric patients for TPE. This retrospective study analyzed data from 39 patients aged from 0 to 18 years who underwent a total of 172 TPE sessions from January 2015 to April 2018 in a tertiary pediatric intensive care unit. Indications for TPE were, in order of frequency, macrophage activation syndrome (28.2%, n = 11), renal transplantation rejection (15.4%, n = 6), liver failure (15.4%, n = 6), Guillain–Barre's syndrome (15%, n = 6), hemolytic uremic syndrome (7.7%, n = 3), acute demyelinating disease (7.7%, n = 3), septic shock (5.1%, n = 2), and intoxication (5.1%, n = 2). No patient had any adverse event related to the TPE during the procedure. The TPE session was ended prematurely in one patient due to insufficient vascular access and lack of blood flow (2.6%). In the long term, thrombosis due to the indwelling central catheter occurred (5.1%, n = 2). TPE appears to be an effective first-stage or supplementary treatment in a variety of diseases, may be safely used in pediatric patients, and there are significant findings that its area of use will increase. In experienced hands and when assessed carefully, it appears that the rate of adverse reactions and vascular access problems may be low enough to be negligible.

Сauses of Dizziness in Patients with Suspected Stroke

2018 ◽  
Vol 7 (3) ◽  
pp. 217-221
Author(s):  
E. V. Shevchenko ◽  
G. R. Ramazanov ◽  
S. S. Petrikov
Keyword(s):  
Magnetic Resonance Imaging ◽  
Magnetic Resonance ◽  
Demyelinating Disease ◽  
Heart Rhythm ◽  
Diagnostic Methods ◽  
Deficiency Anemia ◽  
Resonance Imaging ◽  
Peripheral Vestibulopathy ◽  
Suspected Stroke ◽  
The Brain

Background Acute dizziness may be the only symptom of stroke. Prevalence of this disease among patients with isolated dizziness differs significantly and depends on study design, inclusion criteria and diagnostic methods. In available investigations, we did not find any prospective studies where magnetic resonance imaging, positional maneuvers, and Halmagyi-Curthoys test had been used to clarify a pattern of diseases with isolated acute dizziness and suspected stroke.Aim of study To clarify the pattern of the causes of dizziness in patients with suspected acute stroke.Material and methods We examined 160 patients admitted to N.V. Sklifosovsky Research Institute for Emergency Medicine with suspected stroke and single or underlying complaint of dizziness. All patients were examined with assessment of neurological status, Dix-Hollpike and Pagnini-McClure maneuvers, HalmagyiCurthoys test, triplex scans of brachiocephalic arteries, transthoracic echocardiography, computed tomography (CT) and magnetic resonance imaging (MRI) of the brain with magnetic field strength 1.5 T. MRI of the brain was performed in patients without evidence of stroke by CT and in patients with stroke of undetermined etiology according to the TOAST classification.Results In 16 patients (10%), the cause of dizziness was a disease of the brain: ischemic stroke (n=14 (88%)), hemorrhage (n=1 (6%)), transient ischemic attack (TIA) of posterior circulation (n=1 (6%)). In 70.6% patients (n=113), the dizziness was associated with peripheral vestibulopathy: benign paroxysmal positional vertigo (n=85 (75%)), vestibular neuritis (n=19 (17%)), Meniere’s disease (n=7 (6%)), labyrinthitis (n=2 (1,3%)). In 6.9% patients (n=11), the cause of dizziness was hypertensive encephalopathy, 1.9% of patients (n=3) had heart rhythm disturbance, 9.4% of patients (n=15) had psychogenic dizziness, 0.6% of patients (n=1) had demyelinating disease, and 0.6% of patients (n=1) had hemic hypoxia associated with iron deficiency anemia.Conclusion In 70.6% patients with acute dizziness, admitted to hospital with a suspected stroke, peripheral vestibulopathy was revealed. Only 10% of patients had a stroke as a cause of dizziness.

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