scholarly journals Selected Biomarkers of Tick-Borne Encephalitis: A Review

2021 ◽  
Vol 22 (19) ◽  
pp. 10615
Author(s):  
Monika Gudowska-Sawczuk ◽  
Barbara Mroczko
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Clinical Decision Making ◽  
White Blood Cells ◽  
Clinical Decision ◽  
Second Phase ◽  
Inflammatory Reactions ◽  
Tick Borne Encephalitis ◽  
Pubmed Database ◽  
The Central Nervous System

Tick-borne encephalitis (TBE) is an acute disease caused by the tick-borne encephalitis virus. Due to the viral nature of the condition, there is no effective causal treatment for full-blown disease. Current and nonspecific TBE treatments only relieve symptoms. Unfortunately, the first phase of TBE is characterized by flu-like symptoms, making diagnosis difficult during this period. The second phase is referred to as the neurological phase as it involves structures in the central nervous system—most commonly the meninges and, in more severe cases, the brain and the spinal cord. Therefore, it is important that early markers of TBE that will guide clinical decision-making and the choice of treatment are established. In this review, we performed an extensive search of literature reports relevant to biomarkers associated with TBE using the MEDLINE/PubMed database. We observed that apart from routinely determined specific immunoglobulins, free light chains may also be useful in the evaluation of intrathecal synthesis in the central nervous system (CNS) during TBEV infection. Moreover, selected metalloproteinases, chemokines, or cytokines appear to play an important role in the pathogenesis of TBE as a consequence of inflammatory reactions and recruitment of white blood cells into the CNS. Furthermore, we reported promising findings on tau protein or Toll-like receptors. It was also observed that some people may be predisposed to TBE. Therefore, to understand the role of selected tick-borne encephalitis biomarkers, we categorized these factors and discussed their potential application in the diagnosis, prognosis, monitoring, or management of TBE.

Emigration of neutrophils in the central nervous system

1983 ◽  
Vol 41 ◽  
pp. 788-789
Author(s):  
John L.Beggs ◽  
John D. Waggener ◽  
Wanda Miller ◽  
Jane Watkins
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Osmium Tetroxide ◽  
White Blood Cells ◽  
Arterial Perfusion ◽  
E Coli ◽  
Intracisternal Injection ◽  
The Central Nervous System ◽  
Brain And Spinal Cord ◽  
Interendothelial Junctions

Studies using mesenteric and ear chamber preparations have shown that interendothelial junctions provide the route for neutrophil emigration during inflammation. The term emigration refers to the passage of white blood cells across the endothelium from the vascular lumen. Although the precise pathway of transendo- thelial emigration in the central nervous system (CNS) has not been resolved, the presence of different physiological and morphological (tight junctions) properties of CNS endothelium may dictate alternate emigration pathways.To study neutrophil emigration in the CNS, we induced meningitis in guinea pigs by intracisternal injection of E. coli bacteria.In this model, leptomeningeal inflammation is well developed by 3 hr. After 3 1/2 hr, animals were sacrificed by arterial perfusion with 3% phosphate buffered glutaraldehyde. Tissues from brain and spinal cord were post-fixed in 1% osmium tetroxide, dehydrated in alcohols and propylene oxide, and embedded in Epon. Thin serial sections were cut with diamond knives and examined in a Philips 300 electron microscope.

CHAPTER 9: Immunology of TBEV-Infections

2020 ◽  
Keyword(s):  
Central Nervous System ◽  
T Cells ◽  
Cerebrospinal Fluid ◽  
Nervous System ◽  
Nk Cells ◽  
Peripheral Blood ◽  
Sample Collection ◽  
Tick Borne Encephalitis ◽  
Viral Infectious Disease ◽  
The Central Nervous System

Tick-borne encephalitis (TBE) is a viral infectious disease of the central nervous system caused by the tick-borne encephalitis virus (TBEV). TBE is usually a biphasic disease and in humans the virus can only be detected during the first (unspecific) phase of the disease. Pathogenesis of TBE is not well understood, but both direct viral effects and immune-mediated tissue damage of the central nervous system may contribute to the natural course of TBE. The effect of TBEV on the innate immune system has mainly been studied in vitro and in mouse models. Characterization of human immune responses to TBEV is primarily conducted in peripheral blood and cerebrospinal fluid, due to the inaccessibility of brain tissue for sample collection. Natural killer (NK) cells and T cells are activated during the second (meningo-encephalitic) phase of TBE. The potential involvement of other cell types has not been examined to date. Immune cells from peripheral blood, in particular neutrophils, T cells, B cells and NK cells, infiltrate into the cerebrospinal fluid of TBE patients.

Chapter 9: Immunology of TBEV-Infection

2021 ◽  
Author(s):  
Sara Gredmark-Russ ◽  
Renata Varnaite
Keyword(s):  
Central Nervous System ◽  
T Cells ◽  
Cerebrospinal Fluid ◽  
Nervous System ◽  
Nk Cells ◽  
Peripheral Blood ◽  
Sample Collection ◽  
Tick Borne Encephalitis ◽  
Viral Infectious Disease ◽  
The Central Nervous System

Tick-borne encephalitis (TBE) is a viral infectious disease of the central nervous system caused by the tick-borne encephalitis virus (TBEV). TBE is usually a biphasic disease and in humans the virus can only be detected during the first (unspecific) phase of the disease. Pathogenesis of TBE is not well understood, but both direct viral effects and immune-mediated tissue damage of the central nervous system may contribute to the natural course of TBE. The effect of TBEV on the innate immune system has mainly been studied in vitro and in mouse models. Characterization of human immune responses to TBEV is primarily conducted in peripheral blood and cerebrospinal fluid, due to the inaccessibility of brain tissue for sample collection. Natural killer (NK) cells and T cells are activated during the second (meningo-encephalitic) phase of TBE. The potential involvement of other cell types has not been examined to date. Immune cells from peripheral blood, in particular neutrophils, T cells, B cells and NK cells, infiltrate into the cerebrospinal fluid of TBE patients.

Сellular and Molecular Mechanisms of Proinflammatory Monocytes Participation in the Pathogenesis of Mental Disorders. Part 3

Psychiatry ◽  
2021 ◽  
Vol 19 (4) ◽  
pp. 125-134
Author(s):  
E. F. Vasilyeva ◽  
O. S. Brusov
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Mental Disorders ◽  
Molecular Mechanisms ◽  
Microglial Cells ◽  
Inflammatory Reactions ◽  
Mental Diseases ◽  
The Central Nervous System ◽  
The Brain

Background: at present, the important role of the monocyte-macrophage link of immunity in the pathogenesis of mental diseases has been determined. In the first and second parts of our review, the cellular and molecular mechanisms of activation of monocytes/macrophages, which secreting proinflammatory CD16 receptors, cytokines, chemokines and receptors to them, in the development of systemic immune inflammation in the pathogenesis of somatic diseases and mental disorders, including schizophrenia, bipolar affective disorder (BAD) and depression were analyzed. The association of high levels of proinflammatory activity of monocytes/macrophages in patients with mental disorders with somatic comorbidity, including immune system diseases, is shown. It is known that proinflammatory monocytes of peripheral blood, as a result of violation of the integrity of the hematoencephalic barrier can migrate to the central nervous system and activate the resident brain cells — microglia, causing its activation. Activation of microglia can lead to the development of neuroinammation and neurodegenerative processes in the brain and, as a result, to cognitive disorders. The aim of review: to analyze the results of the main scientific studies concerning the role of cellular and molecular mechanisms of peripheral blood monocytes interaction with microglial cells and platelets in the development of neuroinflammation in the pathogenesis of mental disorders, including Alzheimer’s disease (AD). Material and methods: keywords “mental disorders, AD, proinflammatory monocytes, microglia, neuroinflammation, cytokines, chemokines, cell adhesion molecules, platelets, microvesicles” were used to search for articles of domestic and foreign authors published over the past 30 years in the databases PubMed, eLibrary, Science Direct and EMBASE. Conclusion: this review analyzes the results of studies which show that monocytes/macrophages and microglia have similar gene expression profiles in schizophrenia, BAD, depression, and AD and also perform similar functions: phagocytosis and inflammatory responses. Monocytes recruited to the central nervous system stimulate the increased production of proinflammatory cytokines IL-1, IL-6, tumor necrosis factor alpha (TNF-α), chemokines, for example, MCP-1 (Monocyte chemotactic protein-1) by microglial cells. This promotes the recruitment of microglial cells to the sites of neuronal damage, and also enhances the formation of the brain protein beta-amyloid (Aβ). The results of modern studies are presented, indicating that platelets are involved in systemic inflammatory reactions, where they interact with monocytes to form monocyte-platelet aggregates (MTA), which induce the activation of monocytes with a pro inflammatory phenotype. In the last decade, it has been established that activated platelets and other cells of the immune system, including monocytes, detached microvesicles (MV) from the membrane. It has been shown that MV are involved as messengers in the transport of biologically active lipids, cytokines, complement, and other molecules that can cause exacerbation of systemic inflammatory reactions. The presented review allows us to expand our knowledge about the cellular and molecular aspects of the interaction of monocytes/macrophages with microglial cells and platelets in the development of neuroinflammation and cognitive decline in the pathogenesis of mental diseases and in AD, and also helps in the search for specific biomarkers of the clinical severity of mental disorder in patients and the prospects for their response to treatment.

The Kinetics of Sodium Transfer in the Central Nervous System of the Cockroach, Periplaneta Americana L

1961 ◽  
Vol 38 (4) ◽  
pp. 737-746
Author(s):  
J. E. TREHERNE
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Periplaneta Americana ◽  
Slow Phase ◽  
Second Phase ◽  
Sodium Ions ◽  
Rapid Phase ◽  
Fast Phase ◽  
The Central Nervous System ◽  
Sodium Extrusion

1. The exchange of sodium ions in the cockroach central nervous system has been studied by following the escape of 24Na from isolated abdominal nerve cords, single connectives and ganglia. Particular attention was paid to the initial rapid exchanges of sodium. 2. The escape of sodium ions occurred as a two-stage process, an initial rapid phase eventually giving way to a slower exponential phase of sodium loss. The fast phase of efflux was not affected by the presence of 2:4-dinitrophenol, although this poison significantly reduced the second slow phase of sodium extrusion. 3. The initial fast phase is attributed to a rapid diffusion from an extracellular space, demonstrated by 14C-inulin; the second phase is identified as the slower extrusion from the cellular components of the central nervous system.

scholarly journals The Role of Catheter Angiography in the Diagnosis of Central Nervous System Vasculitis

2016 ◽  
Vol 5 (3-4) ◽  
pp. 194-208 ◽  
Author(s):  
Randall C. Edgell ◽  
Ahmed E. Sarhan ◽  
Jazba Soomro ◽  
Collin Einertson ◽  
Joanna Kemp ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Clinical Decision Making ◽  
Case Series ◽  
Low Frequency ◽  
Catheter Angiography ◽  
Central Nervous System Vasculitis ◽  
Diagnostic Challenge ◽  
Pubmed Database ◽  
Angiographic Findings

Background: Central nervous system vasculitis (CNSV) is a rare disorder, the pathophysiology of which is not fully understood. It involves a combination of inflammation and thrombosis. CNSV is most commonly associated with headache, gradual changes in mental status, and focal neurological symptoms. Diagnosis requires the effective use of history, laboratory testing, imaging, and biopsy. Catheter angiography can be a powerful tool in the diagnosis when common and low-frequency angiographic manifestations of CNSV are considered. We review these manifestations and their place in the diagnostic algorithm of CNSV. Summary: We reviewed the PubMed database for case series of CNSV that included 5 or more patients. Demographic and angiographic findings were collected. Angiographic findings were dichotomized between common and low-frequency findings. A system for incorporating these findings into clinical decision-making is proposed. Key Message: CNSV is a diagnostic challenge due to the absence of a true gold standard test. In the absence of such a test, catheter angiography remains a central piece of the diagnostic puzzle when appropriately employed and interpreted.

scholarly journals Central nervous system filariasis masquerading as a glioma: case report

2017 ◽  
Vol 127 (3) ◽  
pp. 691-693 ◽  
Author(s):  
Adesh Shrivastava ◽  
Prateek Arora ◽  
Akriti Khare ◽  
Garima Goel ◽  
Neelkamal Kapoor
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Histopathological Examination ◽  
Interesting Case ◽  
Filarial Infection ◽  
Provisional Diagnosis ◽  
Inflammatory Reactions ◽  
Neoplastic Lesions ◽  
The Central Nervous System ◽  
Glioma Case

Filariasis, an endemic zoonosis in the Southeast Asia region, has been reported to affect various organs as well as the central nervous system (CNS). Inflammatory reactions mimicking those from neoplastic lesions clinically and radiologically have been reported in the breast and urinary bladder. To date, a CNS manifestation of filarial infestation has been reported in the form of meningoencephalitis. The authors here present an interesting case of a young man presenting in status epilepticus, which on radiological evaluation appeared to be a glioma. However, postoperative histopathological examination changed the provisional diagnosis to a filarial infection of the CNS mimicking a primary CNS neoplasm.

Climate, ticks and tick-borne encephalitis in Central Europe.

2021 ◽  
pp. 331-340
Author(s):  
Vlasta Danielová ◽  
Milan Daniel
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Central Europe ◽  
Human Disease ◽  
European Area ◽  
Tick Borne Encephalitis ◽  
The Family ◽  
The Central Nervous System ◽  
Tick Borne Encephalitis Virus ◽  
European Subtype

Abstract Tick-borne encephalitis (TBE) is a serious human disease of the central nervous system (CNS) caused by the European subtype of tick-borne encephalitis virus (TBEV) - genus Flavivirus of the family Flaviviridae - in the European area of its distribution. Its major vector is the tick, Ixodes ricinus. This expert opinion discusses the ecology of I. ricinus and the epidemiology of TBE in relation to changing climate in Central Europe.

scholarly journals Assessment of the YKL-40 concentration in patients with tick-borne encephalitis

2020 ◽  
Author(s):  
Piotr Czupryna ◽  
Agnieszka Kulczyńka-Przybik ◽  
Barbara Mroczko ◽  
Mulugeta Wondim ◽  
Sambor Grygorczuk ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Early Stage ◽  
Central Nervous System Involvement ◽  
Control Group ◽  
Roc Curve Analysis ◽  
Group I ◽  
Tick Borne Encephalitis ◽  
The Central Nervous System ◽  
Tick Borne Encephalitis Virus

Abstract Background Tick-Borne Encephalitis (TBE) is a viral infection of the Central Nervous System (CNS) caused by Tick-Borne Encephalitis Virus (TBEV). It might take several clinical courses such as: meningitis, meningoencephalitis or meningoencephalomyelitis. The aim this study was to compare the YKL-40 concentration in cerebrospinal fluid (CSF) of patients with different clinical presentations of TBE and patients with excluded meningitis (control group). Methods The concentration of YKL-40 in CSF was determined using Fujirebio tests (Ghent, Belgium) in 32 patients with TBE: group I—patients with meningoencephalitis (n = 16); group II—patients with meningitis (n = 16). The control group (CG) consisted of 17 patients in whom inflammatory process in central nervous system was excluded. Results The concentration of YKL-40 was significantly higher in encephalitis group than in CG after 7 days from the last dose of treatment. The concentration in patients with neuroinflammation had significantly different concentration of YKL-40 compared to patients with no neuroinflammation control groups. ROC curve analysis indicates that: CSF YKL-40 concentration at cut off 783.87 differentiated TBE patients from CG with 100% specificity and 70% sensitivity and CSF YKL-40 concentration at cut off 980.11 differentiated meningitis from meningoencephalitis with 87.5% specificity and 62.5% sensitivity. Conclusions YKL-40 takes part in TBE pathogenesis, its concentration is the highest at the early stage of Central Nervous System involvement and decreases in the convalescent period. As YKL-40 is significantly higher in meningitis than in meningoencephalitis, it might be used as biomarker in differentiation of these clinical forms of TBE.

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