scholarly journals Influence of systemic immune responses in the brain after wound injury of tail amputation in zebrafish

2020 ◽  
Vol 16 (S3) ◽  
Author(s):  
Xiang‐Ke Chen ◽  
Alvin Chun‐Hang Ma ◽  
Raymond Chuen‐Chung Chang
Keyword(s):  
Immune Responses ◽  
The Brain

scholarly journals Evidence for Differential Roles for NKG2D Receptor Signaling in Innate Host Defense against Coronavirus-Induced Neurological and Liver Disease

2007 ◽  
Vol 82 (6) ◽  
pp. 3021-3030 ◽  
Author(s):  
Kevin B. Walsh ◽  
Melissa B. Lodoen ◽  
Robert A. Edwards ◽  
Lewis L. Lanier ◽  
Thomas E. Lane
Keyword(s):  
Liver Disease ◽  
Immune Responses ◽  
Host Defense ◽  
Nk Cell ◽  
Hepatitis Virus ◽  
Innate Immune ◽  
Liver Pathology ◽  
Innate Immune Responses ◽  
Ifn Γ ◽  
The Brain

ABSTRACT Infection of SCID mice with a recombinant murine coronavirus (mouse hepatitis virus [MHV]) expressing the T-cell chemoattractant CXC chemokine ligand 10 (CXCL10) resulted in increased survival and reduced viral burden within the brain and liver compared to those of mice infected with an isogenic control virus (MHV), supporting an important role for CXCL10 in innate immune responses following viral infection. Enhanced protection in MHV-CXCL10-infected mice correlated with increased gamma interferon (IFN-γ) production by infiltrating natural killer (NK) cells within the brain and reduced liver pathology. To explore the underlying mechanisms associated with protection from disease in MHV-CXCL10-infected mice, the functional contributions of the NK cell-activating receptor NKG2D in host defense were examined. The administration of an NKG2D-blocking antibody to MHV-CXCL10-infected mice did not reduce survival, dampen IFN-γ production in the brain, or affect liver pathology. However, NKG2D neutralization increased viral titers within the liver, suggesting a protective role for NKG2D signaling in this organ. These data indicate that (i) CXCL10 enhances innate immune responses, resulting in protection from MHV-induced neurological and liver disease; (ii) elevated NK cell IFN-γ expression in the brain of MHV-CXCL10-infected mice occurs independently of NKG2D; and (iii) NKG2D signaling promotes antiviral activity within the livers of MHV-infected mice that is not dependent on IFN-γ and tumor necrosis factor alpha secretion.

scholarly journals The Peptide Vaccine Combined with Prior Immunization of a Conventional Diphtheria-Tetanus Toxoid Vaccine Induced AmyloidβBinding Antibodies on Cynomolgus Monkeys and Guinea Pigs

2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Akira Yano ◽  
Kaori Ito ◽  
Yoshikatsu Miwa ◽  
Yoshito Kanazawa ◽  
Akiko Chiba ◽  
...  
Keyword(s):  
Immune Responses ◽  
Tetanus Toxoid ◽  
Guinea Pigs ◽  
Peptide Vaccine ◽  
Cell Epitope ◽  
T Cell Epitope ◽  
Peptide Vaccination ◽  
Binding Profile ◽  
Cynomolgus Monkeys ◽  
The Brain

The reduction of brain amyloid beta (Aβ) peptides by anti-Aβantibodies is one of the possible therapies for Alzheimer’s disease. We previously reported that the Aβpeptide vaccine including the T-cell epitope of diphtheria-tetanus combined toxoid (DT) induced anti-Aβantibodies, and the prior immunization with conventional DT vaccine enhanced the immunogenicity of the peptide. Cynomolgus monkeys were given the peptide vaccine subcutaneously in combination with the prior DT vaccination. Vaccination with a similar regimen was also performed on guinea pigs. The peptide vaccine induced anti-Aβantibodies in cynomolgus monkeys and guinea pigs without chemical adjuvants, and excessive immune responses were not observed. Those antibodies could preferentially recognize Aβ40, and Aβ42compared to Aβfibrils. The levels of serum anti-Aβantibodies and plasma Aβpeptides increased in both animals and decreased the brain Aβ40level of guinea pigs. The peptide vaccine could induce a similar binding profile of anti-Aβantibodies in cynomolgus monkeys and guinea pigs. The peptide vaccination could be expected to reduce the brain Aβpeptides and their toxic effects via clearance of Aβpeptides by generated antibodies.

scholarly journals Stability of Lentiviral Vector-Mediated Transgene Expression in the Brain in the Presence of Systemic Antivector Immune Responses

2005 ◽  
Vol 16 (6) ◽  
pp. 741-751 ◽  
Author(s):  
Evelyn Abordo-Adesida ◽  
Antonia Follenzi ◽  
Carlos Barcia ◽  
Sandra Sciascia ◽  
Maria G. Castro ◽  
...  
Keyword(s):  
Immune Responses ◽  
Transgene Expression ◽  
Lentiviral Vector ◽  
The Brain

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 Psychoneuroimmunoendocrinology and Immune Homeostasis: Gut-brain Axis, Obesity and Cognitive Function

2020 ◽  
Vol 6 (12) ◽  
pp. 124-154
Author(s):  
S. Bulgakova ◽  
N. Romanchuk ◽  
O. Pomazanova
Keyword(s):  
Artificial Intelligence ◽  
Health Care ◽  
Gut Microbiota ◽  
Immune Responses ◽  
Cognitive Functions ◽  
Immune Homeostasis ◽  
Obesity And Diabetes ◽  
Human Immune ◽  
The Cross ◽  
The Brain

The new competencies of psychoneuroimmunoendocrinology and psychoneuroimmunology play a strategic role in interdisciplinary science and interdisciplinary planning and decision-making. The introduction of multi-vector neurotechnologies of artificial intelligence and the principles of digital health care will contribute to the development of modern neuroscience and neuromarketing. The availability of innovative technologies, such as next-generation sequencing and correlated bioinformatics tools, allows deeper investigation of the cross-network relationships between the microbiota and human immune responses. Immune homeostasis is the balance between immunological tolerance and inflammatory immune responses — a key feature in the outcome of health or disease. A healthy microbiota is the qualitative and quantitative ratio of diverse microbes of individual organs and systems, maintaining the biochemical, metabolic and immune equilibrium of the macroorganism necessary to preserve human health. Functional foods, healthy biomicrobiota, healthy lifestyle and controlled protective environmental effects, artificial intelligence and electromagnetic information load/overload are responsible for the work of the human immune system and its ability to respond to pandemic attacks in a timely manner. Obesity continues to be one of the main problems of modern health care due to its high prevalence and polymorbidity. In addition to cardiometabolic diseases, lesions of the musculoskeletal system, obese individuals show impaired cognitive functions, have a high risk of developing depression and anxiety. The gut microbiota mediates between environmental influences (food, lifestyle) and the physiology of the host, and its change may partially explain the cross-link between the above pathologies. It is known that Western eating patterns are the main cause of the obesity epidemic, which also contributes to dysbiotic drift of the gut microbiota, which in turn contributes to the development of complications associated with obesity. Experimental studies in animal models and, to a lesser extent in humans, show that microbiota is associated with obesity and may contribute to the endocrine, neurochemical and development of systemic inflammation underlying obesity itself and related diseases. Nevertheless, a number of questions remain at present. Modeling the microbiota-gut-brain axis, provides the brain with information from the gut not only through the nervous system but also through a continuous stream of microbial, endocrine, metabolic and immune messages. The communication network provides important keys to understanding how obesity and diabetes can affect the brain by provoking neuropsychiatric diseases. The literature review is devoted to the analysis of data on the relationship of the gut-brain axis, obesity and cognitive functions, immune homeostasis and new competencies: psychoneuroimmunology and psychoneuroimmunoendocrinology.

scholarly journals Syk and Hrs Regulate TLR3-Mediated Antiviral Response in Murine Astrocytes

2019 ◽  
Vol 2019 ◽  
pp. 1-21 ◽  
Author(s):  
Matylda B. Mielcarska ◽  
Magdalena Bossowska-Nowicka ◽  
Karolina P. Gregorczyk-Zboroch ◽  
Zbigniew Wyżewski ◽  
Lidia Szulc-Dąbrowska ◽  
...  
Keyword(s):  
Immune Responses ◽  
Signaling Pathway ◽  
Critical Role ◽  
Antiviral Response ◽  
Proteolytic Processing ◽  
Viral Dsrna ◽  
Kinase Substrate ◽  
Tlr3 Signaling ◽  
The Brain

Toll-like receptors (TLRs) sense the presence of pathogen-associated molecular patterns. Nevertheless, the mechanisms modulating TLR-triggered innate immune responses are not yet fully understood. Complex regulatory systems exist to appropriately direct immune responses against foreign or self-nucleic acids, and a critical role of hepatocyte growth factor-regulated tyrosine kinase substrate (HRS), endosomal sorting complex required for transportation-0 (ESCRT-0) subunit, has recently been implicated in the endolysosomal transportation of TLR7 and TLR9. We investigated the involvement of Syk, Hrs, and STAM in the regulation of the TLR3 signaling pathway in a murine astrocyte cell line C8-D1A following cell stimulation with a viral dsRNA mimetic. Our data uncover a relationship between TLR3 and ESCRT-0, point out Syk as dsRNA-activated kinase, and suggest the role for Syk in mediating TLR3 signaling in murine astrocytes. We show molecular events that occur shortly after dsRNA stimulation of astrocytes and result in Syk Tyr-342 phosphorylation. Further, TLR3 undergoes proteolytic processing; the resulting TLR3 N-terminal form interacts with Hrs. The knockdown of Syk and Hrs enhances TLR3-mediated antiviral response in the form of IFN-β, IL-6, and CXCL8 secretion. Understanding the role of Syk and Hrs in TLR3 immune responses is of high importance since activation and precise execution of the TLR3 signaling pathway in the brain seem to be particularly significant in mounting an effective antiviral defense. Infection of the brain with herpes simplex type 1 virus may increase the secretion of amyloid-β by neurons and astrocytes and be a causal factor in degenerative diseases such as Alzheimer’s disease. Errors in TLR3 signaling, especially related to the precise regulation of the receptor transportation and degradation, need careful observation as they may disclose foundations to identify novel or sustain known therapeutic targets.

scholarly journals Cerebral sterile inflammation in neurodegenerative diseases

2020 ◽  
Vol 40 (1) ◽  
Author(s):  
Kento Otani ◽  
Takashi Shichita
Keyword(s):  
Immune Responses ◽  
Neurodegenerative Diseases ◽  
Molecular Mechanisms ◽  
Therapeutic Agents ◽  
Sterile Inflammation ◽  
Cellular Damage ◽  
Cellular Mechanisms ◽  
Abnormal Accumulation ◽  
The Brain ◽  
Lateral Sclerosis

AbstractTherapeutic strategies for regulating neuroinflammation are expected in the development of novel therapeutic agents to prevent the progression of central nervous system (CNS) pathologies. An understanding of the detailed molecular and cellular mechanisms of neuroinflammation in each CNS disease is necessary for the development of therapeutics. Since the brain is a sterile organ, neuroinflammation in Alzheimer’s disease (AD), Parkinson’s disease (PD), and amyotrophic lateral sclerosis (ALS) is triggered by cerebral cellular damage or the abnormal accumulation of inflammatogenic molecules in CNS tissue through the activation of innate and acquired immunity. Inflammation and CNS pathologies worsen each other through various cellular and molecular mechanisms, such as oxidative stress or the accumulation of inflammatogenic molecules induced in the damaged CNS tissue. In this review, we summarize the recent evidence regarding sterile immune responses in neurodegenerative diseases.

scholarly journals Pavlovian Conditioning of Immunological and Neuroendocrine Functions

2020 ◽  
Vol 100 (1) ◽  
pp. 357-405 ◽  
Author(s):  
Martin Hadamitzky ◽  
Laura Lückemann ◽  
Gustavo Pacheco-López ◽  
Manfred Schedlowski
Keyword(s):  
Immune Responses ◽  
Associative Learning ◽  
Animal Studies ◽  
Research Field ◽  
Immune Functions ◽  
Humoral Immune ◽  
Central Nervous System Activity ◽  
New Research ◽  
The Brain ◽  
Neuroendocrine Functions

The phenomenon of behaviorally conditioned immunological and neuroendocrine functions has been investigated for the past 100 yr. The observation that associative learning processes can modify peripheral immune functions was first reported and investigated by Ivan Petrovic Pavlov and his co-workers. Their work later fell into oblivion, also because so little was known about the immune system’s function and even less about the underlying mechanisms of how learning, a central nervous system activity, could affect peripheral immune responses. With the employment of a taste-avoidance paradigm in rats, this phenomenon was rediscovered 45 yr ago as one of the most fascinating examples of the reciprocal functional interaction between behavior, the brain, and peripheral immune functions, and it established psychoneuroimmunology as a new research field. Relying on growing knowledge about efferent and afferent communication pathways between the brain, neuroendocrine system, primary and secondary immune organs, and immunocompetent cells, experimental animal studies demonstrate that cellular and humoral immune and neuroendocrine functions can be modulated via associative learning protocols. These (from the classical perspective) learned immune responses are clinically relevant, since they affect the development and progression of immune-related diseases and, more importantly, are also inducible in humans. The increased knowledge about the neuropsychological machinery steering learning and memory processes together with recent insight into the mechanisms mediating placebo responses provide fascinating perspectives to exploit these learned immune and neuroendocrine responses as supportive therapies, the aim being to reduce the amount of medication required, diminishing unwanted drug side effects while maximizing the therapeutic effect for the patient’s benefit.

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