Mesocestoides corti intracranial infection as a murine model for neurocysticercosis

Parasitology ◽  
2010 ◽  
Vol 137 (3) ◽  
pp. 359-372 ◽  
Author(s):  
JORGE I. ALVAREZ ◽  
BIBHUTI B. MISHRA ◽  
UMA MAHESH GUNDRA ◽  
PRAMOD K. MISHRA ◽  
JUDY M. TEALE
Keyword(s):  
Immune Responses ◽  
Murine Model ◽  
Taenia Solium ◽  
Toll Like Receptor ◽  
Therapeutic Approaches ◽  
Larval Form ◽  
The Central Nervous System ◽  
Receptor Signaling Pathway ◽  
Kinetics Of ◽  
The Brain

SUMMARYNeurocysticercosis (NCC) is the most common parasitic disease of the central nervous system (CNS) caused by the larval form of the tapeworm Taenia solium. NCC has a long asymptomatic period with little or no inflammation, and the sequential progression to symptomatic NCC depends upon the intense inflammation associated with degeneration of larvae. The mechanisms involved in these progressive events are difficult to study in human patients. Thus it was necessary to develop an experimental model that replicated NCC. In this review, we describe studies of a murine model of NCC in terms of the release/secretion of parasite antigens, immune responses elicited within the CNS environment and subsequent pathogenesis. In particular, the kinetics of leukocyte subsets infiltrating into the brain are discussed in the context of disruption of the CNS barriers at distinct anatomical sites and the mechanisms contributing to these processes. In addition, production of various inflammatory mediators and the mechanisms involved in their induction by the Toll-like receptor signaling pathway are described. Overall, the knowledge gained from the mouse model of NCC has provided new insights for understanding the kinetics of events contributing to different stages of NCC and should aid in the formulation of more effective therapeutic approaches.

scholarly journals Replication Kinetics, Cell Tropism, and Associated Immune Responses in SARS-CoV-2- and H5N1 Virus-Infected Human Induced Pluripotent Stem Cell-Derived Neural Models

mSphere ◽  
2021 ◽  
Author(s):  
Lisa Bauer ◽  
Bas Lendemeijer ◽  
Lonneke Leijten ◽  
Carmen W. E. Embregts ◽  
Barry Rockx ◽  
...  
Keyword(s):  
Immune Responses ◽  
H5n1 Virus ◽  
Induced Pluripotent Stem Cell ◽  
Neurological Complications ◽  
Olfactory Nerve ◽  
Cell Tropism ◽  
Neural Models ◽  
The Central Nervous System ◽  
Induced Pluripotent ◽  
The Brain

Infections with the recently emerged severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) are often associated with neurological complications. Evidence suggests that SARS-CoV-2 enters the brain via the olfactory nerve; however, SARS-CoV-2 is only rarely detected in the central nervous system of COVID-19 patients.

scholarly journals Multiple Parenchymal Neurocysticercosis: A Case Report

2012 ◽  
Vol 10 (1) ◽  
pp. 44-45 ◽  
Author(s):  
I KC ◽  
KJ Rana ◽  
R Joshi ◽  
A Mandal ◽  
S Bhhatarai
Keyword(s):  
Rare Case ◽  
Taenia Solium ◽  
Parasitic Infection ◽  
Brain Parenchyma ◽  
Larval Form ◽  
Cns Involvement ◽  
Huge Number ◽  
Adult Tapeworm ◽  
The Brain ◽  
Multiple Cysts

Cysticercosis is a parasitic infection with CNS involvement in 60-90% of infested patients. The larval form of pork intestinal tapeworm (Taenia solium) is responsible for cysticercosis. Humans are the definitive hosts and usually harbor the adult tapeworm in small intestine as an asymptomatic infestation. Neurocysticercosis most commonly affects the brain parenchyma. Solitary and multiple cysts in brain parencyma is common but we came across a 24 year old lady patient with huge number of cysts which is relatively rare. The aim of this article is to report the rare case. DOI: http://dx.doi.org/10.3126/mjsbh.v10i1.6450 Medical Journal of Shree Birendra Hospital Jan-June 2011 10(1) 44-45

Urea transport in the central nervous system

1962 ◽  
Vol 203 (4) ◽  
pp. 739-747 ◽  
Author(s):  
Charles R. Kleeman ◽  
Hugh Davson ◽  
Emanuel Levin
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Nervous Tissue ◽  
Urea Transport ◽  
Major Barrier ◽  
Rate Of Penetration ◽  
The Central Nervous System ◽  
Kinetics Of ◽  
The Brain ◽  
State Content

The kinetics of urea transport in the central nervous system have been studied in rabbits during sustained intravenous and intracisternal infusions of C12 and C14 urea. The steady state content of urea in the water phase of the white matter and cord was approximately equal to its content in plasma water. However, the water of whole brain and gray matter had levels of urea which exceeded those in plasma by 7 and 18%, respectively, whereas the urea in cerebrospinal fluid (CSF) was only 78% of the plasma level. Its rate of penetration into nervous tissue was approximately one-tenth as rapid as into muscle. The intravenous infusion of urea caused a significant decrease in water content of the brain and cord. It was estimated that urea infused into the subarachnoid space penetrated the central nervous system (CNS) tissues at four to five times the rate of transport from blood to CNS tissues. These studies suggest that intravenous infusions of urea lower CSF pressure by decreasing the volume of the brain and cord. The major barrier to urea penetration into nervous tissue is at the capillary level, and not the plasma membrane of the glial or neuronal cells.

scholarly journals “Corneal Nerves, CD11c+ Dendritic Cells and Their Impact on Ocular Immune Privilege”

2021 ◽  
Vol 12 ◽  
Author(s):  
Jerry Y. Niederkorn
Keyword(s):  
Immune Responses ◽  
Inflammatory Diseases ◽  
Innate Immune ◽  
Immune Privilege ◽  
Innate Immune Responses ◽  
Regulatory Processes ◽  
Immune Mediated ◽  
Corneal Nerves ◽  
The Central Nervous System ◽  
The Brain

The eye and the brain have limited capacities for regeneration and as such, immune-mediated inflammation can produce devastating consequences in the form of neurodegenerative diseases of the central nervous system or blindness as a result of ocular inflammatory diseases such as uveitis. Accordingly, both the eye and the brain are designed to limit immune responses and inflammation – a condition known as “immune privilege”. Immune privilege is sustained by physiological, anatomical, and regulatory processes that conspire to restrict both adaptive and innate immune responses.

scholarly journals Neuropathogenesis caused by Trypanosoma brucei, still an enigma to be unveiled

2021 ◽  
Vol 8 (4) ◽  
pp. 73-76
Author(s):  
Katherine Figarella
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Immune Responses ◽  
Trypanosoma Brucei ◽  
Late Stage ◽  
Early Stage ◽  
Tropical Diseases ◽  
The Central Nervous System ◽  
The Impact ◽  
The Brain

Trypanosoma brucei is one of the protozoa parasites that can enter the brain and cause injury associated with toxic effects of parasite-derived molecules or with immune responses against infection. Other protozoa parasites with brain tropism include Toxoplasma, Plasmodium, Amoeba, and, eventually, other Trypano-somatids such as T. cruzi and Leishmania. Together, these parasites affect billions of people worldwide and are responsible for more than 500.000 deaths annually. Factors determining brain tropism, mechanisms of in-vasion as well as processes ongoing inside the brain are not well understood. But, they depend on the par-asite involved. The pathogenesis caused by T. brucei initiates locally in the area of parasite inoculation, soon trypanosomes rich the blood, and the disease enters in the so-called early stage. The pathomecha-nisms in this phase have been described, even mole-cules used to combat the disease are effective during this period. Later, the disease evolves towards a late-stage, characterized by the presence of parasites in the central nervous system (CNS), the so-called meningo-encephalitic stage. This phase of the disease has not been sufficiently examined and remains a matter of investigation. Here, I stress the importance of delve into the study of the neuropathogenesis caused by T. brucei, which will enable the identification of path-ways that may be targeted to overcome parasites that reached the CNS. Finally, I highlight the impact that the application of tools developed in the last years in the field of neuroscience will have on the study of neglect-ed tropical diseases.

scholarly journals Role of Neuroinflammation in Adult Neurogenesis and Alzheimer Disease: Therapeutic Approaches

2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
Almudena Fuster-Matanzo ◽  
María Llorens-Martín ◽  
Félix Hernández ◽  
Jesús Avila
Keyword(s):  
Immune Response ◽  
Alzheimer Disease ◽  
Adult Neurogenesis ◽  
The Elderly ◽  
Therapeutic Approaches ◽  
Common Cause ◽  
The Central Nervous System ◽  
Chronic Activation ◽  
The Brain

Neuroinflammation, a specialized immune response that takes place in the central nervous system, has been linked to neurodegenerative diseases, and specially, it has been considered as a hallmark of Alzheimer disease, the most common cause of dementia in the elderly nowadays. Furthermore, neuroinflammation has been demonstrated to affect important processes in the brain, such as the formation of new neurons, commonly known as adult neurogenesis. For this, many therapeutic approaches have been developed in order to avoid or mitigate the deleterious effects caused by the chronic activation of the immune response. Considering this, in this paper we revise the relationships between neuroinflammation, Alzheimer disease, and adult neurogenesis, as well as the current therapeutic approaches that have been developed in the field.

scholarly journals Cerebral cysticercosis in Campina Grande, Paraíba - northern Brazil: computerized tomography diagnosis importance

1996 ◽  
Vol 54 (1) ◽  
pp. 94-97 ◽  
Author(s):  
Thiago D. Gonçalves-Coêlho ◽  
Matheus Diniz G. Coelho
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Endemic Area ◽  
Taenia Solium ◽  
Larval Form ◽  
Cysticercus Cellulosae ◽  
Pedro I ◽  
The Central Nervous System ◽  
Cerebral Cysticercosis ◽  
Northern Brazil

Neurocysticercosis is the infection of the central nervous system by the larval form of Taenia solium , the Cysticercus cellulosae. We studied 4011 computerized tomographies performed in TomoHPI Radioimaging Service, Hospital Pedro I, Campina Grande PB, Northern Brazil, since its installation on August 1993 to July 1995. 41 patients were diagnosed as having Cysticercus cerebral infestation, corresponding to an incidence of 1.02%. No cases were related in Campina Grande PB during 1991 according to hospitalizations under prospective payment rates. After this radioimaging service installation, we observed 1.86 cases per month. We conclude that Campina Grande has to be included as an endemic area of neurocysticercosis, needing health service measures to cease the cycle Taenia-Cysticercus, the only way to get rid of such a serious problem.

Plasmacytoid dendritic cells and autoimmune inflammation

2014 ◽  
Vol 395 (3) ◽  
pp. 335-346 ◽  
Author(s):  
Georgina Galicia ◽  
Jennifer L. Gommerman
Keyword(s):  
Dendritic Cells ◽  
Immune Responses ◽  
Plasmacytoid Dendritic Cells ◽  
Type I ◽  
Toll Like Receptor ◽  
Autoimmune Encephalomyelitis ◽  
Effector Cells ◽  
The Central Nervous System ◽  
Antigen Presenting ◽  
Experimental Autoimmune

Abstract Plasmacytoid dendritic cells (pDC) are a sub-population of dendritic cells (DC) that produce large amounts of type I interferon (IFN) in response to nucleic acids that bind and activate toll-like-receptor (TLR)9 and TLR7. Type I IFN can regulate the function of B, T, DC, and natural killer (NK) cells and can also alter the residence time of leukocytes within lymph nodes. Activated pDC can also function as antigen presenting cells (APC) and have the potential to prime and differentiate T cells into regulatory or inflammatory effector cells, depending on the context. In this review we discuss pDC ontogeny, function, trafficking, and activation. We will also examine how pDC can potentially be involved in regulating immune responses in the periphery as well as within the central nervous system (CNS) during multiple sclerosis (MS) and its animal model, experimental autoimmune encephalomyelitis (EAE).

Distribution and histopathological changes induced by cysts ofTaenia soliumin the brain of pigs from Tanzania

2014 ◽  
Vol 89 (5) ◽  
pp. 559-564 ◽  
Author(s):  
E.M. Mkupasi ◽  
H.A. Ngowi ◽  
C.S. Sikasunge ◽  
P.S. Leifsson ◽  
M.V. Johansen
Keyword(s):  
Parietal Lobe ◽  
Taenia Solium ◽  
Clinical Signs ◽  
Occipital Lobe ◽  
Loss Of Consciousness ◽  
Parasitic Disease ◽  
Histopathological Changes ◽  
The Central Nervous System ◽  
Spinal Cord Cysts ◽  
The Brain

AbstractNeurocysticercosis (NCC) caused byTaenia soliumcysts is a frequent but neglected parasitic disease of the central nervous system (CNS) worldwide. The aim of this study was to describe anatomical locations of cysts in the CNS and the corresponding inflammation. A total of 17 naturally infected pigs were used to evaluate the distribution of cysts and, of these, seven were used to evaluate the corresponding inflammation further, through histopathology. Clinical signs in the pigs included dullness, sluggishness, somnolence, apathy and loss of consciousness. Cysts were distributed in all cerebral lobes, i.e. 39.7% in the frontal lobe, 20.3% in the parietal lobe, 20.0% in the occipital lobe and 19.7% in the temporal lobe, and only 0.4% in the cerebellum. No cysts were found in the spinal cord. Cysts were localized as follows: 47.9% in the dorsal subarachnoid, 46.9% in the parenchyma, 4.4% in the subarachnoid base and 0.9% in the ventricles. The results of the histopathology revealed lesions in an early inflammatory stage, i.e. stage I, in all anatomical locations except for two, which showed more of an inflammatory reaction, stage III, in one pig. It was concluded that clinical signs in pigs were neither pathognomonic nor consistent. These signs, therefore, cannot be used as a reliable indicator of porcine NCC. Furthermore,T. soliumcysts were found to be in abundance in all cerebral lobes, and only a few were found in the cerebellum. Regarding the inflammatory response, no significant differences were found in the location and total number of cysts. Thus, further studies are needed to explain the determinants of cyst distribution in the CNS and assess in detail clinical signs associated with porcine NCC.

Effects of Neuroinflammation on Neural Stem Cells

2016 ◽  
Vol 23 (1) ◽  
pp. 27-39 ◽  
Author(s):  
Ruxandra Covacu ◽  
Lou Brundin
Keyword(s):  
Immune Responses ◽  
Subventricular Zone ◽  
Neurological Diseases ◽  
Experimental Models ◽  
Adaptive Immune ◽  
Neural Stem Progenitor Cells ◽  
The Central Nervous System ◽  
And Migration ◽  
The Brain ◽  
Proliferation And Migration

Neural stem/progenitor cells (NSCs/NPCs) are present in different locations in the central nervous system. In the subgranular zone (SGZ) there is a constant generation of new neurons under normal conditions. New neurons are also formed from the subventricular zone (SVZ) NSCs, and they migrate anteriorly as neuroblast to the olfactory bulb in rodents, whereas in humans migration is directed toward striatum. Most CNS injuries elicit proliferation and migration of the NSCs toward the injury site, indicating the activation of a regenerative response. However, regeneration from NSC is incomplete, and this could be due to detrimental cues encountered during inflammation. Different CNS diseases and trauma cause activation of the innate and adaptive immune responses that influence the NSCs. Furthermore, NSCs in the brain react differently to inflammatory cues than their counterparts in the spinal cord. In this review, we have summarized the effects of inflammation on NSCs in relation to their origin and briefly described the NSC activity during different neurological diseases or experimental models.

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