scholarly journals Neurologic disruption arising from Immunologic Aberration

2019 ◽  
Vol 4 (4) ◽  
pp. 01-05
Author(s):  
Trevor Archer

Interactions between neurodegenerative states and immune system dysregulations may underlie several diseases that induce problems for neuropsychological and physical health. It seems increasingly evident that process of apoptosis, a central issue for health and well-being, is associated to greater or lesser extents with the balance and ongoing regulation of immune system proclivities. One key contributor to the regulation of structure and function of brain and behaviour has emerged to be the gastrointestinal microbiome, not least in the context of the neurodegenerative disorders. Certain genes identified in in these disorders encode for proteins with directly-acting immunoactive/immunoreactive roles, which when mutated lead to dysregulations in immune functions, thereby affecting the disease states; yet accumulating evidence implies direct malfunctions of immune ells in the brain and CNS as well as at the periphery of the nervous system. Remarkably, the therapeutic effects of anti-tumor, immune system-enhancing agents are emerging to awaken the necessity for consideration of immune system-nervous system interactions as reciprocal determinants of both neurodegenerative and inflammatory disorders.

2020 ◽  
Vol 7 (1) ◽  
pp. 1-23 ◽  
Author(s):  
Eloisa Salvo-Romero ◽  
Patricia Stokes ◽  
Mélanie G. Gareau

The vast diversity of bacteria that inhabit the gastrointestinal tract strongly influence host physiology, not only nutrient metabolism but also immune system development and function. The complexity of the microbiota is matched by the complexity of the host immune system, where they have coevolved to maintain homeostasis ensuring the mutualistic host-microbial relationship. Numerous studies in recent years investigating the gut-brain axis have demonstrated an important role for the gut microbiota in modulating brain development and function, with the immune system serving as an important coordinator of these interactions. Gut bacteria can modulate not only gut-resident immune cells but also brain-resident immune cells. Activation of the immune system in the gut and in the brain are implicated in responses to neuroinflammation, brain injury, as well as changes in neurogenesis and plasticity. Impairments in this bidirectional communication are implicated in the etiopathogenesis of psychiatric and neurodevelopmental diseases and disorders, including autism spectrum disorders, or comorbidities associated with Gastrointestinal diseases, including inflammatory bowel diseases, where dysbiosis is commonly seen. Consequently, probiotics, or beneficial microbes, are being recognized as promising therapeutic targets to modulate behavior and brain development by modulating the gut microbiota. Here we review the role of microbiota-immune interactions in the gut and the brain during homeostasis and disease and their impact on gut-brain communication, brain function, and behavior as well as the use of probiotics in central nervous system alterations. Statement of novelty: The microbiota-gut-brain axis is increasingly recognized as an important physiological pathway for maintaining health and impacting the brain and central nervous system. Increasing evidence suggests that the immune system is crucial for gut-brain signaling. In this review, we highlight the critical studies in the literature that identify the key immune pathways involved.


Author(s):  
William H. Walker II ◽  
A. Courtney DeVries

Neuroimmunology is the study of the interaction between the immune system and nervous system during development, homeostasis, and disease states. Descriptions of neuroinflammatory diseases dates back centuries. However, in depth scientific investigation in the field began in the late 19th century and continues into the 21st century. Contrary to prior dogma in the field of neuroimmunology, there is immense reciprocal crosstalk between the brain and the immune system throughout development, homeostasis, and disease states. Proper neuroimmune functioning is necessary for optimal health, as the neuroimmune system regulates vital processes including neuronal signaling, synapse pruning, and clearance of debris and pathogens within the central nervous system. Perturbations in optimal neuroimmune functioning can have detrimental consequences for the host and underlie a myriad of physical, cognitive, and behavioral abnormalities. As such, the field of neuroimmunology is still relatively young and dynamic and represents an area of active research and discovery.


2014 ◽  
Vol 222 (3) ◽  
pp. 148-153 ◽  
Author(s):  
Sabine Vits ◽  
Manfred Schedlowski

Associative learning processes are one of the major neuropsychological mechanisms steering the placebo response in different physiological systems and end organ functions. Learned placebo effects on immune functions are based on the bidirectional communication between the central nervous system (CNS) and the peripheral immune system. Based on this “hardware,” experimental evidence in animals and humans showed that humoral and cellular immune functions can be affected by behavioral conditioning processes. We will first highlight and summarize data documenting the variety of experimental approaches conditioning protocols employed, affecting different immunological functions by associative learning. Taking a well-established paradigm employing a conditioned taste aversion model in rats with the immunosuppressive drug cyclosporine A (CsA) as an unconditioned stimulus (US) as an example, we will then summarize the efferent and afferent communication pathways as well as central processes activated during a learned immunosuppression. In addition, the potential clinical relevance of learned placebo effects on the outcome of immune-related diseases has been demonstrated in a number of different clinical conditions in rodents. More importantly, the learned immunosuppression is not restricted to experimental animals but can be also induced in humans. These data so far show that (i) behavioral conditioned immunosuppression is not limited to a single event but can be reproduced over time, (ii) immunosuppression cannot be induced by mere expectation, (iii) psychological and biological variables can be identified as predictors for this learned immunosuppression. Together with experimental approaches employing a placebo-controlled dose reduction these data provide a basis for new therapeutic approaches to the treatment of diseases where a suppression of immune functions is required via modulation of nervous system-immune system communication by learned placebo effects.


1994 ◽  
Vol 31 (1) ◽  
pp. 48-54 ◽  
Author(s):  
J. F. Edwards ◽  
R. W. Storts ◽  
J. R. Joyce ◽  
J. M. Shelton ◽  
C. S. Menzies

Two, 8-month-old Rambouillet half-sister ewes with signs of visual loss and decreased mentation were examined. Ewe No. 1 was necropsied at 10 months of age, and alter being held under observation for a further 6 months, ewe No. 2 was necropsied at 16 months of age. At that time, the ewe was blind and severely depressed. Both ewes had deposition of an autofluorescent lipopigment, identified as ceroid-lipofuscin, in neurons of the brain, spinal cord, eye, and dorsal root ganglia. The disease process was progressive and characterized by deposition of lipopigment with neuronal degeneration and severe fibrillary aslrogliosis. This progressive loss of neurons in the older ewe led to severe retinal degeneration. No pigment was observed in cells outside of the nervous system and eye. Controlled breeding studies have shown that this disease has an autosomal, recessive inheritance. The disease referred to here as juvenile-onset neuronal ceroid-lipofuscinosis of Rambouillet sheep is unlike the majority of the hereditary ceroid-lipofuscinoses that occur in human beings and animals in that only the nervous system is affected. Therefore, this disease could serve as an excellent model for the study of lipopigment deposition that affects the nervous system as a result of various disease states and during aging.


1978 ◽  
Vol 49 (1) ◽  
pp. 84-92 ◽  
Author(s):  
Robert A. Morantz ◽  
William Shain ◽  
Humberto Cravioto

✓ The theory of immune surveillance postulates that one function of the immune system is to eliminate small numbers of malignant cells that arise spontaneously within the organism. Although there has been a great deal of both clinical and experimental evidence in favor of this theory as it applies to general oncology, the question of whether or not such a surveillance system would be effective for tumors arising within the nervous system has never been studied. The young of pregnant rats which had been exposed to the neurocarcinogen ethylnitrosourea (ENU) were divided into control, immunosuppressed, and immunoenhanced groups. These lifetime alterations of the immune system had no effect on the course of nervous system tumor formation. We believe that the most likely explanation for our results is that the “immunological privilege” of the brain prevents the usual interaction of the neoplasm and the immune system from occurring.


Author(s):  
Georgia E. Hodes

In the late 20th century, the discovery that the immune system and central nervous system were not autonomous revolutionized exploration of the mechanisms by which stress contributes to immune disorders and immune regulation contributes to mental illness. There is increasing evidence of stress as integrated across the brain and body. The immune system acts in concert with the peripheral nervous system to shape the brain’s perception of the environment. The brain in turn communicates with the endocrine and immune systems to guide their responses to that environment. Examining the groundwork of mechanisms governing communication between the body and brain will hopefully provide a better understanding of the ontogeny and symptomology of some mood disorders.


2018 ◽  
Vol 94 (1114) ◽  
pp. 446-452 ◽  
Author(s):  
Borros M Arneth

BackgroundThe gut–brain axis facilitates a critical bidirectional link and communication between the brain and the gut. Recent studies have highlighted the significance of interactions in the gut–brain axis, with a particular focus on intestinal functions, the nervous system and the brain. Furthermore, researchers have examined the effects of the gut microbiome on mental health and psychiatric well-being.The present study reviewed published evidence to explore the concept of the gut–brain axis.AimsThis systematic review investigated the relationship between human brain function and the gut–brain axis.MethodsTo achieve these objectives, peer-reviewed articles on the gut–brain axis were identified in various electronic databases, including PubMed, MEDLINE, CIHAHL, Web of Science and PsycINFO.ResultsData obtained from previous studies showed that the gut–brain axis links various peripheral intestinal functions to brain centres through a broad range of processes and pathways, such as endocrine signalling and immune system activation. Researchers have found that the vagus nerve drives bidirectional communication between the various systems in the gut–brain axis. In humans, the signals are transmitted from the liminal environment to the central nervous system.ConclusionsThe communication that occurs in the gut–brain axis can alter brain function and trigger various psychiatric conditions, such as schizophrenia and depression. Thus, elucidation of the gut–brain axis is critical for the management of certain psychiatric and mental disorders.


Mr . President and Gentlemen, My most pleasant duty to-day is to thank your Council for the honour that it has conferred upon me by inviting me to give the second lecture in memory of the late Sir David Ferrier. I have accepted this invitation with feelings of gratitude, not only to your Council, but also for the contributions made in this country to our knowledge of the structure and function of the nervous system. Among these, the works of Sir David Ferrier, however prominent, only stand out as a conspicuous example of a national tradition, maintained in recent years, both in the Physiology and Anatomy of the brain. The task I have accepted is not an easy one, the less so as the first Ferrier lecture was given by Sir Charles Sherrington who, in both the methods and results of his investigations, attained a degree of exactness at which morphologists aim in vain.


Cells ◽  
2020 ◽  
Vol 9 (11) ◽  
pp. 2340
Author(s):  
Hannah E. Henson ◽  
Michael R. Taylor

The spliceosome consists of accessory proteins and small nuclear ribonucleoproteins (snRNPs) that remove introns from RNA. As splicing defects are associated with degenerative conditions, a better understanding of spliceosome formation and function is essential. We provide insight into the role of a spliceosome protein U4/U6.U5 tri-snRNP-associated protein 1, or Squamous cell carcinoma antigen recognized by T-cells (Sart1). Sart1 recruits the U4.U6/U5 tri-snRNP complex to nuclear RNA. The complex then associates with U1 and U2 snRNPs to form the spliceosome. A forward genetic screen identifying defects in choroid plexus development and whole-exome sequencing (WES) identified a point mutation in exon 12 of sart1 in Danio rerio (zebrafish). This mutation caused an up-regulation of sart1. Using RNA-Seq analysis, we identified additional upregulated genes, including those involved in apoptosis. We also observed increased activated caspase 3 in the brain and eye and down-regulation of vision-related genes. Although splicing occurs in numerous cells types, sart1 expression in zebrafish was restricted to the brain. By identifying sart1 expression in the brain and cell death within the central nervous system (CNS), we provide additional insights into the role of sart1 in specific tissues. We also characterized sart1’s involvement in cell death and vision-related pathways.


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