scholarly journals Role of CCR2 in Inflammatory Conditions of the Central Nervous System

2014 ◽  
Vol 34 (9) ◽  
pp. 1425-1429 ◽  
Author(s):  
Hannah X Chu ◽  
Thiruma V Arumugam ◽  
Mathias Gelderblom ◽  
Tim Magnus ◽  
Grant R Drummond ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Central Nervous System ◽  
Nervous System ◽  
Ischemic Stroke ◽  
Inflammatory Diseases ◽  
Protective Effects ◽  
Cns Inflammation ◽  
Inflammatory Conditions ◽  
The Central Nervous System ◽  
Effective Development

CC chemokine receptor 2 (CCR2) plays important roles in extravasation and transmigration of monocytes under inflammatory conditions. CCR2 and its ligands have been extensively studied in a range of inflammatory diseases in the central nervous system (CNS), including multiple sclerosis, Alzheimer's disease and ischemic stroke. This brief review summarizes our current understanding of the physiologic and pathologic roles of CCR2, focusing on its involvement in CNS inflammatory diseases. There appears to be a rationale for exploring therapies involving CCR2 inhibition in multiple sclerosis and ischemic stroke, but there is also evidence for immunomodulatory and protective effects of CCR2 activity during CNS inflammation. The critical balance between protective and detrimental roles of CCR2-dependent recruitment of leukocytes must therefore be carefully examined to guide safe and effective development of any therapies involving CCR2 modulation.

scholarly journals Multiple Sclerosis and Evaluation of Vitamin D Effect

2019 ◽  
pp. 1-15
Author(s):  
Zahra Eslamifar ◽  
Behnaz Deihim ◽  
Reza Ghaffaripour
Keyword(s):  
Multiple Sclerosis ◽  
Central Nervous System ◽  
Vitamin D ◽  
Nervous System ◽  
Common Ground ◽  
Inflammatory Diseases ◽  
Cognitive Disorders ◽  
Definitive Treatment ◽  
Disease Modifying Drugs ◽  
The Central Nervous System

Multiple sclerosis is an autoimmune disease of the central nervous system with symptoms of neurodegenerative diseases. The symptoms vary depending on damage location. Some of the symptoms include cognitive disorders, anxiety and depression, visual impairment, respiratory, speech and swallowing disorders, muscle spasm and fatigue. Due to the lack of a definitive treatment method, various therapeutic approaches are proposed to control the disease. Drugs are classified into attack control drugs, complication control drugs and disease-modifying drugs. Vitamin D is a hormone-like steroidal compound with immune modulatory and anti-inflammatory properties. Vitamin D deficiency is associated with a variety of inflammatory, neurologic and autoimmune diseases. Many studies on patients as well as experimental autoimmune encephalomyelitis studies have shown that the administration of vitamin D reduces inflammation in inflammatory diseases of the central nervous system. As argued, vitamin D level was significantly lower in MS compared to healthy subjects as controls.  Also, a higher level of vitamin D is reported in relapsing-remitting MS patients compared to patients with progressive MS. It is observed that higher serum levels of vitamin D can reduce the severity of symptoms, progress, and also delays the relapses. Few studies considered vitamin D to be ineffective in stopping or inhibition the disease. Despite the controversies concerning the role of vitamin D in MS progress, there is a lot of interest in further research in this regard with the hope of reaching a common ground. Therefore, frequent reviews of past and recent studies are essential to achieve the same results.

First Presentation of an Acquired Demyelinating Syndrome

2017 ◽  
Vol 16 (03) ◽  
pp. 164-170
Author(s):  
Rachel Gottlieb-Smith ◽  
Amy Waldman
Keyword(s):  
Multiple Sclerosis ◽  
Central Nervous System ◽  
Nervous System ◽  
Differential Diagnosis ◽  
Optic Neuritis ◽  
Clinical Features ◽  
Neuromyelitis Optica ◽  
Transverse Myelitis ◽  
Acute Disseminated Encephalomyelitis ◽  
The Central Nervous System

AbstractAcquired demyelinating syndromes (ADS) present with acute or subacute monofocal or polyfocal neurologic deficits localizing to the central nervous system. The clinical features of distinct ADS have been carefully characterized including optic neuritis, transverse myelitis, and acute disseminated encephalomyelitis. These disorders may all be monophasic disorders. Alternatively, optic neuritis, partial transverse myelitis, and acute disseminated encephalomyelitis may be first presentations of a relapsing or polyphasic neuroinflammatory disorder, such as multiple sclerosis or neuromyelitis optica. The clinical features of these disorders and the differential diagnosis are discussed in this article.

MULTIPLE SCLEROSIS IN CHILDREN

PEDIATRICS ◽  
1958 ◽  
Vol 21 (5) ◽  
pp. 703-709
Author(s):  
John C. Gall ◽  
Alvin B. Hayles ◽  
Robert G. Siekert ◽  
Haddow M. Keith
Keyword(s):  
Multiple Sclerosis ◽  
Central Nervous System ◽  
Nervous System ◽  
Mayo Clinic ◽  
Spinal Fluid ◽  
Neurologic Deficits ◽  
The Central Nervous System ◽  
Physical Findings

Forty cases of disease of the central nervous system, characterized by several episodes and disseminated lesions, with onset in childhood and clinically typical of multiple sclerosis, were studied. The disease as it occurs in children does not appear to differ clinically from the disease as observed in adults, in respect to mode of onset, symptoms, physical findings, and changes in the spinal fluid. In the Mayo Clinic series, however, almost twice as many girls as boys were affected. A pediatrician confronted with a child showing evidence of scattered neurologic deficits that remit, particularly a disturbance of vision and co-ordination, should consider the possibility of multiple sclerosis.

AIM2 inflammasome activation in astrocytes occurs during the late phase of EAE

2021 ◽  
Author(s):  
William E. Barclay ◽  
M. Elizabeth Deerhake ◽  
Makoto Inoue ◽  
Toshiaki Nonaka ◽  
Kengo Nozaki ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Central Nervous System ◽  
Animal Model ◽  
Cell Death ◽  
Nervous System ◽  
Experimental Autoimmune Encephalomyelitis ◽  
Inflammasome Activation ◽  
Autoimmune Encephalomyelitis ◽  
The Central Nervous System ◽  
Experimental Autoimmune

ABSTRACTInflammasomes are a class of innate immune signaling platforms that activate in response to an array of cellular damage and pathogens. Inflammasomes promote inflammation under many circumstances to enhance immunity against pathogens and inflammatory responses through their effector cytokines, IL-1β and IL-18. Multiple sclerosis and its animal model, experimental autoimmune encephalomyelitis (EAE), are such autoimmune conditions influenced by inflammasomes. Despite work investigating inflammasomes during EAE, little remains known concerning the role of inflammasomes in the central nervous system (CNS) during the disease. Here we use multiple genetically modified mouse models to monitor activated inflammasomes in situ based on ASC oligomerization in the spinal cord. Using inflammasome reporter mice, we found heightened inflammasome activation in astrocytes after the disease peak. In contrast, microglia and CNS-infiltrated myeloid cells had few activated inflammasomes in the CNS during EAE. Astrocyte inflammasome activation was dependent on AIM2, but low IL-1β expression and no significant signs of cell death were found in astrocytes during EAE. Thus, the AIM2 inflammasome activation in astrocytes may have a distinct role from traditional inflammasome-mediated inflammation.SIGNIFICANCE STATEMENTInflammasome activation in the peripheral immune system is pathogenic in multiple sclerosis (MS) and its animal model, experimental autoimmune encephalomyelitis (EAE). However, inflammasome activity in the central nervous system (CNS) is largely unexplored. Here, we used genetically modified mice to determine inflammasome activation in the CNS during EAE. Our data indicated heightened AIM2 inflammasome activation in astrocytes after the disease peak. Unexpectedly, neither CNS-infiltrated myeloid cells nor microglia were the primary cells with activated inflammasomes in SC during EAE. Despite AIM2 inflammasome activation, astrocytes did not undergo apparent cell death and produced little of the proinflammatory cytokine, IL-1β, during EAE. This study showed that CNS inflammasome activation occurs during EAE without associating with IL-1β-mediated inflammation.

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