scholarly journals Chlamydia pneumoniae Infection of the Central Nervous System Worsens Experimental Allergic Encephalitis

2002 ◽  
Vol 196 (12) ◽  
pp. 1639-1644 ◽  
Author(s):  
Caigan Du ◽  
Song-Yi Yao ◽  
Åsa Ljunggren-Rose ◽  
Subramaniam Sriram
Keyword(s):  
Multiple Sclerosis ◽  
Central Nervous System ◽  
Nervous System ◽  
Chlamydia Pneumoniae ◽  
Systemic Infection ◽  
Experimental Allergic Encephalitis ◽  
The Central Nervous System ◽  
Severity Of The Disease ◽  
Experimental Allergic ◽  
Intraperitoneal Inoculation

Experimental allergic encephalitis (EAE) is considered by many to be a model for human multiple sclerosis. Intraperitoneal inoculation of mice with Chlamydia pneumoniae, after immunization with neural antigens, increased the severity of EAE. Accentuation of EAE required live infectious C. pneumoniae, and the severity of the disease was attenuated with antiinfective therapy. After immunization with neural antigens, systemic infection with C. pneumoniae led to the dissemination of the organism into the central nervous system (CNS) in mice with accentuated EAE. Inoculation with Chlamydia trachomatis did not worsen EAE and infectious organisms were not seen in the CNS. These observations suggest that dissemination of C. pneumoniae results in localized infection in CNS tissues in animals with EAE. We propose that infection of the CNS by C. pneumoniae can amplify the autoreactive pool of lymphocytes and regulate the expression of an autoimmune disease.

Chlamydia pneumoniae in the cerebrospinal fluid of patients with multiple sclerosis and neurological controls

2001 ◽  
Vol 7 (6) ◽  
pp. 371-374 ◽  
Author(s):  
S Sotgiu ◽  
A Piana ◽  
M Pugliatti ◽  
A Sotgiu ◽  
G A Deiana ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Central Nervous System ◽  
Cerebrospinal Fluid ◽  
Nervous System ◽  
Chlamydia Pneumoniae ◽  
Immunofluorescence Microscopy ◽  
Antibody Detection ◽  
Common Event ◽  
Neurological Patients ◽  
The Central Nervous System

Chlamydia pneumoniae infection is a common event in neurological patients and recovery of C. pneumoniae DNA in the cerebrospinal fluids (CSF) of multiple sclerosis (MS) patients could represent an epiphenomenon. We assessed the relevance of C. pneumoniae infection in 62 CSF samples from 32 MS patients and 30 neurological controls by means of PCR, immunofluorescence microscopy, enzyme-linked fluorescence and antibody detection. Multiple sclerosis (9.3%) and neurological controls (13.3) had similar percentage of anti-C. pneumoniae antibodies. However, C. pneumoniae DNA was only detectable in MS patients' CSF (9.3%). Our data support the hypothesis that C. pneumoniae persistence in some MS patients may be the result of an impaired clearance within the central nervous system.

Chlamydia pneumoniae infection of the central nervous system in multiple sclerosis

1999 ◽  
Vol 46 (1) ◽  
pp. 6-14 ◽  
Author(s):  
Subramaniam Sriram ◽  
Charles W. Stratton ◽  
Song-Yi Yao ◽  
Anthony Tharp ◽  
Lingmei Ding ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Central Nervous System ◽  
Nervous System ◽  
Chlamydia Pneumoniae ◽  
The Central Nervous System

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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