scholarly journals Immunoceptive inference: why are psychiatric disorders and immune responses intertwined?

2021 ◽  
Vol 36 (3) ◽  
Author(s):  
Anjali Bhat ◽  
Thomas Parr ◽  
Maxwell Ramstead ◽  
Karl Friston
Keyword(s):  
Immune System ◽  
Immune Responses ◽  
Psychiatric Disorders ◽  
Message Passing ◽  
Genetic Mutations ◽  
Active Inference ◽  
Sensory Attenuation ◽  
The Brain ◽  
Neuropsychiatric Conditions

AbstractThere is a steadily growing literature on the role of the immune system in psychiatric disorders. So far, these advances have largely taken the form of correlations between specific aspects of inflammation (e.g. blood plasma levels of inflammatory markers, genetic mutations in immune pathways, viral or bacterial infection) with the development of neuropsychiatric conditions such as autism, bipolar disorder, schizophrenia and depression. A fundamental question remains open: why are psychiatric disorders and immune responses intertwined? To address this would require a step back from a historical mind–body dualism that has created such a dichotomy. We propose three contributions of active inference when addressing this question: translation, unification, and simulation. To illustrate these contributions, we consider the following questions. Is there an immunological analogue of sensory attenuation? Is there a common generative model that the brain and immune system jointly optimise? Can the immune response and psychiatric illness both be explained in terms of self-organising systems responding to threatening stimuli in their external environment, whether those stimuli happen to be pathogens, predators, or people? Does false inference at an immunological level alter the message passing at a psychological level (or vice versa) through a principled exchange between the two systems?

Immune and Inflammatory Responses to Stroke: Good Or Bad?

2008 ◽  
Vol 3 (4) ◽  
pp. 254-265 ◽  
Author(s):  
P. A. McCombe ◽  
S. J. Read
Keyword(s):  
Immune Response ◽  
Immune System ◽  
Immune Responses ◽  
Inflammatory Responses ◽  
Tissue Injury ◽  
Therapeutic Option ◽  
Regulatory Lymphocytes ◽  
The Brain ◽  
Pro Inflammatory Cytokines

Inflammatory and immune responses play important roles following ischaemic stroke. Inflammatory responses contribute to damage and also contribute to repair. Injury to tissue triggers an immune response. This is initiated through activation of the innate immune system. In stroke there is microglial activation. This is followed by an influx of lymphocytes and macrophages into the brain, triggered by production of pro-inflammatory cytokines. This inflammatory response contributes to further tissue injury. There is also a systemic immune response to stroke, and there is a degree of immunosuppression that may contribute to the stroke patient's risk of infection. This immunosuppressive response may also be protective, with regulatory lymphocytes producing cytokines and growth factors that are neuroprotective. The specific targets of the immune response after stroke are not known, and the details of the immune and inflammatory responses are only partly understood. The role of inflammation and immune responses after stroke is twofold. The immune system may contribute to damage after stroke, but may also contribute to repair processes. The possibility that some of the immune response after stroke may be neuroprotective is exciting and suggests that deliberate enhancement of these responses may be a therapeutic option.

scholarly journals Distribution of leukocyte subpopulation among students threatened by failure

2020 ◽  
Vol 11 (3) ◽  
pp. 3807-3812
Author(s):  
Aziez Chettoum ◽  
Kamilia Guedri ◽  
Zouhir Djerrou ◽  
Rachid Mosbah ◽  
Latifa Khattabi ◽  
...  
Keyword(s):  
Immune System ◽  
White Blood Cells ◽  
Significant Development ◽  
Biological Assays ◽  
Cell Counts ◽  
Student Volunteers ◽  
White Blood Cell Counts ◽  
Academic Year ◽  
The Brain

Psychoneuroimmunology or the study of the relationships between the brain and the immune system is an area of research that has experienced significant development over the decade. Stress does not appear without consequences on the state of health, the role of fears, emotions and significant constraints in the appearance of organic and mental diseases. In this research, we studied the effect of stress and anxiety during exams at the end of the academic year (2018/2019) on the distribution of leukocyte subpopulations and the immune system, questionnaires has been completed by student volunteers, to estimate the anxio-depressive comorbidities through the (HADS) test during and outside exams, and in the same time we asked them for a blood sample the next morning day to carry out some biological assays (CBC). We also found that stress during exams caused a change in the distribution of different types of white blood cells, a total decrease in white blood cell counts with neutropenia and lymphopenia were found in students during exams compared to controls, and an increase in monocyte and other types of polymorphonuclear levels in students during exams compared to controls. Other tests measuring the effects of stress on specific functions of the immune system can be used.

scholarly journals Role of Immunity in Pathogenesis of Psychosis

2021 ◽  
Author(s):  
Wafa Abdelghaffar ◽  
Oussama Sidhom ◽  
Lilia Laadhar ◽  
Rym Rafrafi
Keyword(s):  
Mental Health ◽  
Immune System ◽  
Psychiatric Symptoms ◽  
Scientific Evidence ◽  
Health Conditions ◽  
Future Research ◽  
Antineuronal Antibodies ◽  
System Components ◽  
The Brain

The involvement of immunity in the pathogenesis of schizophrenia and related psychoses was suspected a century ago but was shadowed by the dopaminergic hypothesis after the discovery of antipsychotics. We currently know that this latter theory has many limits and cannot account for the wide variety of psychotic conditions. The immune-inflammatory theory is now one of the most promising axes of research in terms of pathogenesis of several mental health conditions. Immunity and inflammation play a role at least in a subgroup of patients with psychosis. The immune system is complex with a variety of components and mediators that can all have effects on the brain and thus mediate psychiatric symptoms. In this chapter we will explore the scientific evidence of the role of immune system in pathophysiology of psychosis. The sections of this chapter will discuss the role of innate system components (cytokines, microglia, inflammation.), the role of adaptive system (lymphocytes and antibodies) with a section focusing on auto-immunity and particularly antineuronal antibodies. Finally we will discuss how this research can impact patients management and elaborate recommendations for future research.

scholarly journals Regulatory Immune Cells in Idiopathic Pulmonary Fibrosis: Friends or Foes?

2021 ◽  
Vol 12 ◽  
Author(s):  
Chiel van Geffen ◽  
Astrid Deißler ◽  
Markus Quante ◽  
Harald Renz ◽  
Dominik Hartl ◽  
...  
Keyword(s):  
Immune System ◽  
Idiopathic Pulmonary Fibrosis ◽  
Pulmonary Fibrosis ◽  
Immune Responses ◽  
Immune Cells ◽  
Current Knowledge ◽  
Suppressor Cells ◽  
Interstitial Lung Diseases ◽  
Stromal Stem Cells

The immune system is receiving increasing attention for interstitial lung diseases, as knowledge on its role in fibrosis development and response to therapies is expanding. Uncontrolled immune responses and unbalanced injury-inflammation-repair processes drive the initiation and progression of idiopathic pulmonary fibrosis. The regulatory immune system plays important roles in controlling pathogenic immune responses, regulating inflammation and modulating the transition of inflammation to fibrosis. This review aims to summarize and critically discuss the current knowledge on the potential role of regulatory immune cells, including mesenchymal stromal/stem cells, regulatory T cells, regulatory B cells, macrophages, dendritic cells and myeloid-derived suppressor cells in idiopathic pulmonary fibrosis. Furthermore, we review the emerging role of regulatory immune cells in anti-fibrotic therapy and lung transplantation. A comprehensive understanding of immune regulation could pave the way towards new therapeutic or preventive approaches in idiopathic pulmonary fibrosis.

Inflammation and Pruning May Inform Risk to Psychiatric Disorders. Lessons From Large Genetic Data

2017 ◽  
Vol 41 (S1) ◽  
pp. S56-S56
Author(s):  
C. Crisafulli
Keyword(s):  
Psychiatric Disorders ◽  
Molecular Mechanics ◽  
Association Studies ◽  
Molecular Pathway ◽  
Starting Point ◽  
Single Effect ◽  
Competing Interest ◽  
The Brain ◽  
New Hypothesis

BackgroundIt's known that psychiatric disorders are caused to either environmental and genetics factors. Through the years several hypotheses were tested and many genes were screened for association, resulting in a huge amount of data available for the scientific community. Despite that, the molecular mechanics behind psychiatric disorders remains largely unknown. Traditional association studies may be not enough to pinpoint the molecular underpinnings of psychiatric disorder. We tried to applying a methodology that investigates molecular-pathway-analysis that takes into account several genes per time, clustered in consistent molecular groups and may successfully capture the signal of a number of genetic variations with a small single effect on the disease. This approach might reveal more of the molecular basis of psychiatric disorders.Methodsi)We collected data on studies available in literature for the studied disorder (e.g. Schizophrenia, Bipolar Disorder);ii)We extracted a pool of genes that are likely involved with the disease;iii)We used these genes as starting point to map molecular cascades function-linked. The molecular cascades are then analyzed and pathways and sub-pathways, possibly involved with them, are identified and tested for association.Results/discussionWe obtained interesting results. In particular, signals of enrichment (association) were obtained multiple times on the molecular pathway associated with the pruning activity and inflammation. Molecular mechanics related to neuronal pruning were focused as a major and new hypothesis for the pathophysiology of psychiatric disorders and the role of inflammatory events has been extensively investigated in psychiatry. intersting, inflammatory mechanics in the brain may also play a role in neuronal pruning during the early development of CNS.Disclosure of interestThe author has not supplied his declaration of competing interest.

scholarly journals Role of the microbiome in human development

Gut ◽  
2019 ◽  
Vol 68 (6) ◽  
pp. 1108-1114 ◽  
Author(s):  
Maria Gloria Dominguez-Bello ◽  
Filipa Godoy-Vitorino ◽  
Rob Knight ◽  
Martin J Blaser
Keyword(s):  
Immune System ◽  
Immune Responses ◽  
Human Development ◽  
Life Forms ◽  
Host Responses ◽  
Host Immune System ◽  
Next Generation ◽  
Host Health ◽  
Host Development

The host-microbiome supraorganism appears to have coevolved and the unperturbed microbial component of the dyad renders host health sustainable. This coevolution has likely shaped evolving phenotypes in all life forms on this predominantly microbial planet. The microbiota seems to exert effects on the next generation from gestation, via maternal microbiota and immune responses. The microbiota ecosystems develop, restricted to their epithelial niches by the host immune system, concomitantly with the host chronological development, providing early modulation of physiological host development and functions for nutrition, immunity and resistance to pathogens at all ages. Here, we review the role of the microbiome in human development, including evolutionary considerations, and the maternal/fetal relationships, contributions to nutrition and growth. We also discuss what constitutes a healthy microbiota, how antimicrobial modern practices are impacting the human microbiota, the associations between microbiota perturbations, host responses and diseases rocketing in urban societies and potential for future restoration.

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 Diagnostic and Treatment Approaches Involving Transthyretin in Amyloidogenic Diseases

2019 ◽  
Vol 20 (12) ◽  
pp. 2982 ◽  
Author(s):  
Gil Yong Park ◽  
Angelo Jamerlan ◽  
Kyu Hwan Shim ◽  
Seong Soo A. An
Keyword(s):  
Cerebrospinal Fluid ◽  
Genetic Mutations ◽  
Hormone Binding ◽  
Wild Type ◽  
Autonomic Motor ◽  
Hormone Binding Protein ◽  
The Brain ◽  
Tetrameric Form

Transthyretin (TTR) is a thyroid hormone-binding protein which transports thyroxine from the bloodstream to the brain. The structural stability of TTR in tetrameric form is crucial for maintaining its original functions in blood or cerebrospinal fluid (CSF). The altered structure of TTR due to genetic mutations or its deposits due to aggregation could cause several deadly diseases such as cardiomyopathy and neuropathy in autonomic, motor, and sensory systems. The early diagnoses for hereditary amyloid TTR with cardiomyopathy (ATTR-CM) and wild-type amyloid TTR (ATTRwt) amyloidosis, which result from amyloid TTR (ATTR) deposition, are difficult to distinguish due to the close similarities of symptoms. Thus, many researchers investigated the role of ATTR as a biomarker, especially its potential for differential diagnosis due to its varying pathogenic involvement in hereditary ATTR-CM and ATTRwt amyloidosis. As a result, the detection of ATTR became valuable in the diagnosis and determination of the best course of treatment for ATTR amyloidoses. Assessing the extent of ATTR deposition and genetic analysis could help in determining disease progression, and thus survival rate could be improved following the determination of the appropriate course of treatment for the patient. Here, the perspectives of ATTR in various diseases were presented.

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