scholarly journals The immunology of stress and the impact of inflammation on the brain and behaviour

2021 ◽  
pp. 1-8
Author(s):  
Meghna Ravi ◽  
Andrew H. Miller ◽  
Vasiliki Michopoulos
Keyword(s):  
Immune System ◽  
Inflammatory Response ◽  
Depression And Anxiety ◽  
Stress Exposure ◽  
Acute And Chronic Stress ◽  
Chronic Stressors ◽  
Psychiatric Conditions ◽  
Chronic Activation ◽  
The Impact ◽  
The Brain

SUMMARY Exposure to acute versus chronic stressors and threats activates the immune system in adaptive and maladaptive manners respectively. Chronic activation arising from persistent stress exposure can contribute to an inflammatory response in the periphery and in the brain that has been implicated in stress-related psychopathology, including depression and anxiety. We review the immunology of acute and chronic stress exposure, integrate this discussion with the emerging literature linking heightened immune activation and inflammation to mood and anxiety disorders, and consider the translational implications of the immune system's role in these psychiatric conditions, with a brief overview of potential interventions.

Keep Your Brain Tissue Healthy

2021 ◽  
pp. 27-66
Author(s):  
Charles Alessi ◽  
Larry W. Chambers ◽  
Muir Gray
Keyword(s):  
Physical Activity ◽  
Immune System ◽  
Inflammatory Response ◽  
Stress Reduction ◽  
Indirect Effects ◽  
Cognitive Abilities ◽  
Direct And Indirect Effects ◽  
The Impact ◽  
The Brain

This chapter starts by advising how to reduce the impact of stress. When stress becomes long term, the immune system becomes less sensitive to cortisol, and since inflammation is partly regulated by this hormone, this decreased sensitivity heightens the inflammatory response and allows inflammation to get out of control, increasing our risk of many diseases. You can reduce your stress yourself through a variety of methods, including physical activity and mindfulness-based stress reduction. Adequate sleep is also a major factor that can improve cognitive abilities and reduce the risk of dementia, and this chapter outlines what we need to know about sleep cycles, insomnia, and sleep disordered breathing, and how to sleep more and sleep better. The chapter then covers how to protect your brain from over medication (polypharmacy). It finishes by discussing how to maintain and indeed increase your levels of physical activity, and how increasing physical activity has both direct and indirect effects on the brain.

scholarly journals Suppression of the Peripheral Immune System Limits the Central Immune Response Following Cuprizone-Feeding: Relevance to Modelling Multiple Sclerosis

Cells ◽  
2019 ◽  
Vol 8 (11) ◽  
pp. 1314 ◽  
Author(s):  
Sen ◽  
Almuslehi ◽  
Gyengesi ◽  
Myers ◽  
Shortland ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Immune Response ◽  
Immune System ◽  
Adaptive Immune System ◽  
Synaptic Function ◽  
Adaptive Immune ◽  
Splenic Atrophy ◽  
The Impact ◽  
The Brain ◽  
Inside Out

Cuprizone (CPZ) preferentially affects oligodendrocytes (OLG), resulting in demyelination. To investigate whether central oligodendrocytosis and gliosis triggered an adaptive immune response, the impact of combining a standard (0.2%) or low (0.1%) dose of ingested CPZ with disruption of the blood brain barrier (BBB), using pertussis toxin (PT), was assessed in mice. 0.2% CPZ(±PT) for 5 weeks produced oligodendrocytosis, demyelination and gliosis plus marked splenic atrophy (37%) and reduced levels of CD4 (44%) and CD8 (61%). Conversely, 0.1% CPZ(±PT) produced a similar oligodendrocytosis, demyelination and gliosis but a smaller reduction in splenic CD4 (11%) and CD8 (14%) levels and no splenic atrophy. Long-term feeding of 0.1% CPZ(±PT) for 12 weeks produced similar reductions in CD4 (27%) and CD8 (43%), as well as splenic atrophy (33%), as seen with 0.2% CPZ(±PT) for 5 weeks. Collectively, these results suggest that 0.1% CPZ for 5 weeks may be a more promising model to study the ‘inside-out’ theory of Multiple Sclerosis (MS). However, neither CD4 nor CD8 were detected in the brain in CPZ±PT groups, indicating that CPZ-mediated suppression of peripheral immune organs is a major impediment to studying the ‘inside-out’ role of the adaptive immune system in this model over long time periods. Notably, CPZ(±PT)-feeding induced changes in the brain proteome related to the suppression of immune function, cellular metabolism, synaptic function and cellular structure/organization, indicating that demyelinating conditions, such as MS, can be initiated in the absence of adaptive immune system involvement.

scholarly journals Systemic inflammation in hemorrhagic strokes – A novel neurological sign and therapeutic target?

2019 ◽  
Vol 39 (6) ◽  
pp. 959-988 ◽  
Author(s):  
Aisha R Saand ◽  
Fang Yu ◽  
Jun Chen ◽  
Sherry H-Y Chou
Keyword(s):  
Brain Injury ◽  
Inflammatory Response ◽  
Immune Responses ◽  
Systemic Inflammation ◽  
Systemic Disease ◽  
Systemic Inflammatory Response ◽  
Organ Systems ◽  
Novel Therapeutic Strategies ◽  
The Impact ◽  
The Brain

Growing evidences suggest that stroke is a systemic disease affecting many organ systems beyond the brain. Stroke-related systemic inflammatory response and immune dysregulations may play an important role in brain injury, recovery, and stroke outcome. The two main phenomena in stroke-related peripheral immune dysregulations are systemic inflammation and post-stroke immunosuppression. There is emerging evidence suggesting that the spleen contracts following ischemic stroke, activates peripheral immune response and this may further potentiate brain injury. Whether similar brain–immune crosstalk occurs in hemorrhagic strokes such as intracerebral hemorrhage (ICH) and subarachnoid hemorrhage (SAH) is not established. In this review, we systematically examined animal and human evidence to date on peripheral immune responses associated with hemorrhagic strokes. Specifically, we reviewed the impact of clinical systemic inflammatory response syndrome (SIRS), inflammation- and immune-associated biomarkers, the brain–spleen interaction, and cellular mediators of peripheral immune responses to ICH and SAH including regulatory T cells (Tregs). While there is growing data suggesting that peripheral immune dysregulation following hemorrhagic strokes may be important in brain injury pathogenesis and outcome, details of this brain-immune system cross-talk remain insufficiently understood. This is an important unmet scientific need that may lead to novel therapeutic strategies in this highly morbid condition.

Pengaruh Stres Kronik terhadap Otak: Kajian Biomolekuler Hormon Glukokortikoid dan Regulasi Brain-Derived Neurotrophic Factor (BDNF) Pascastres di Cerebellum

2017 ◽  
Vol 9 (2) ◽  
pp. 65
Author(s):  
Desby Juananda ◽  
Dwi Cahyani Ratna Sari ◽  
Djoko Prakosa2, ◽  
Nur Arfian ◽  
Mansyur Romi
Keyword(s):  
Chronic Stress ◽  
Brain Plasticity ◽  
Critical Role ◽  
Synaptic Function ◽  
Bdnf Expression ◽  
Acute And Chronic Stress ◽  
Repetitive Stress ◽  
Central Organ ◽  
The Impact ◽  
The Brain

The brain is the central organ of stress adaptation, and is also a target of stress. Chronic stress may result in abnormalchanges in brain plasticity; include dendritic retraction, neuronal toxicity, and suppression of neurogenesis andaxospinous synaptic plasticity. Repetitive stress exposure will gradually change the electrical characteristic, morphologyand proliferative capacity of neurons. Among brain region, the cerebellum is known to be severely affected by oxidativedamage associated with glucocorticoids level. It is believed due to the highest levels of glucocorticoid receptorslocalized in the external granular layer. BDNF, a member of neurotrophin family, is known to be a strong survivalpromoting factor, and plays a critical role in cell proliferation and differentiation, neuronal protection, and the regulationof synaptic function in the central nervous system. BDNF is highly expressed in the cerebellum, mainly in granulecells. Both acute and chronic stress change BDNF expression in the brain. Although the impact of stress on BDNFlevels showed the different results, BDNF is believed to protect neurons from injuries caused by stress.

scholarly journals Inhibition of Toll-like Receptor and Cytokine Signaling—A Unifying Theme in Ischemic Tolerance

2004 ◽  
Vol 24 (11) ◽  
pp. 1288-1304 ◽  
Author(s):  
Katalin Karikó ◽  
Drew Weissman ◽  
Frank A. Welsh
Keyword(s):  
Immune System ◽  
Inflammatory Response ◽  
Lipid Rafts ◽  
Inflammatory Cytokines ◽  
Innate Immune System ◽  
Endotoxin Tolerance ◽  
Ischemic Tolerance ◽  
Innate Immune ◽  
Cytokine Signaling ◽  
The Brain

Cerebral ischemia triggers acute inflammation, which exacerbates primary brain damage. Activation of the innate immune system is an important component of this inflammatory response. Inflammation occurs through the action of proinflammatory cytokines, such as TNF, IL-1β and IL-6, that alter blood flow and increase vascular permeability, thus leading to secondary ischemia and accumulation of immune cells in the brain. Production of these cytokines is initiated by signaling through Toll-like receptors (TLRs) that recognize host-derived molecules released from injured tissues and cells. Recently, great strides have been made in understanding the regulation of the innate immune system, particularly the signaling mechanisms of TLRs. Negative feedback inhibitors of TLRs and inflammatory cytokines have now been identified and characterized. It is also evident that lipid rafts exist in membranes and play a role in receptor-mediated inflammatory signaling events. In the present review, using this newly available large body of knowledge, we take a fresh look at studies of ischemic tolerance. Based on this analysis, we recognize a striking similarity between ischemic tolerance and endotoxin tolerance, an immune suppressive state characterized by hyporesponsiveness to lipopolysaccharide (LPS). In view of this analogy, and considering recent discoveries related to molecular mechanisms of endotoxin tolerance, we postulate that inhibition of TLR and proinflammatory cytokine signaling contributes critically to ischemic tolerance in the brain and other organs. Ischemic tolerance is a protective mechanism induced by a variety of preconditioning stimuli. Tolerance can be established with two temporal profiles: (i) a rapid form in which the trigger induces tolerance to ischemia within minutes and (ii) a delayed form in which development of protection takes several hours or days and requires de-novo protein synthesis. The rapid form of tolerance is achieved by direct interference with membrane fluidity, causing disruption of lipid rafts leading to inhibition of TLR/cytokine signaling pathways. In the delayed form of tolerance, the preconditioning stimulus first triggers the TLR/cytokine inflammatory pathways, leading not only to inflammation but also to simultaneous upregulation of feedback inhibitors of inflammation. These inhibitors, which include signaling inhibitors, decoy receptors, and anti-inflammatory cytokines, reduce the inflammatory response to a subsequent episode of ischemia. This novel interpretation of the molecular mechanism of ischemic tolerance highlights new avenues for future investigation into the prevention and treatment of stroke and related diseases.

scholarly journals Prophylactic Ketamine Treatment Promotes Resilience to Chronic Stress and Accelerates Recovery: Correlation with Changes in Synaptic Plasticity in the CA3 Subregion of the Hippocampus

2019 ◽  
Vol 20 (7) ◽  
pp. 1726 ◽  
Author(s):  
Adam Krzystyniak ◽  
Ewa Baczynska ◽  
Marta Magnowska ◽  
Svitlana Antoniuk ◽  
Matylda Roszkowska ◽  
...  
Keyword(s):  
Dendritic Spine ◽  
Recovery Period ◽  
Structural Plasticity ◽  
Brain Regions ◽  
Spine Density ◽  
Depression And Anxiety ◽  
Stress Exposure ◽  
Animal Models Of Depression ◽  
Dendritic Spine Morphology ◽  
The Brain

Ketamine is an N-methyl-d-aspartate receptor antagonist that has gained wide attention as a potent antidepressant. It has also been recently reported to have prophylactic effects in animal models of depression and anxiety. Alterations of neuroplasticity in different brain regions; such as the hippocampus; prefrontal cortex; and amygdala; are a hallmark of stress-related disorders; and such changes may endure beyond the treatment of symptoms. The present study investigated whether a prophylactic injection of ketamine has effects on structural plasticity in the brain in mice that are subjected to chronic unpredictable stress followed by an 8-day recovery period. Ketamine administration (3 mg/kg body weight) 1 h before stress exposure increased the number of resilient animals immediately after the cessation of stress exposure and positively influenced the recovery of susceptible animals to hedonic deficits. At the end of the recovery period; ketamine-treated animals exhibited significant differences in dendritic spine density and dendritic spine morphology in brain regions associated with depression compared with saline-treated animals. These results confirm previous findings of the prophylactic effects of ketamine and provide further evidence of an association between the antidepressant-like effect of ketamine and alterations of structural plasticity in the brain

scholarly journals Stress-Related Brain Neuroinflammation Impact in Depression: Role of the Corticotropin-Releasing Hormone System and P2X7 Receptor

2021 ◽  
pp. 1-9
Author(s):  
Susana Silberstein ◽  
Ana Clara Liberman ◽  
Paula Ayelén dos Santos Claro ◽  
Maria Belén Ugo ◽  
Jan M. Deussing ◽  
...  
Keyword(s):  
P2x7 Receptor ◽  
Immune Functions ◽  
Inflammatory Pathways ◽  
Treatment Of Depression ◽  
Inflammatory Processes ◽  
Psychiatric Conditions ◽  
The Impact ◽  
The Brain ◽  
Hormone System

Depression and other psychiatric stress-related disorders are leading causes of disability worldwide. Up to date, treatments of mood disorders have limited success, most likely due to the multifactorial etiology of these conditions. Alterations in inflammatory processes have been identified as possible pathophysiological mechanisms in psychiatric conditions. Here, we review the main features of 2 systems involved in the control of these inflammatory pathways: the CRH system as a key regulator of the stress response and the ATP-gated ion-channel P2X7 receptor (P2X7R) involved in the control of immune functions. The pathophysiology of depression as a stress-related psychiatric disorder is depicted in terms of the impact of CRH and P2X7R function on inflammatory pathways in the brain. Understanding pathogenesis of affective disorders will lead to the development of therapies for treatment of depression and other stress-related diseases.

scholarly journals Immunonutrition and surgical practice

1999 ◽  
Vol 58 (4) ◽  
pp. 831-837 ◽  
Author(s):  
Leán O'Flaherty ◽  
David J. Bouchier-Hayes
Keyword(s):  
Immune System ◽  
Inflammatory Response ◽  
Acute Phase ◽  
Acute Phase Response ◽  
Biological Properties ◽  
Normal Function ◽  
Phase Response ◽  
Nutrition Support ◽  
Major Surgery ◽  
The Impact

Immunonutrition generally refers to the effect of the provision of specific nutrients on the immune system. These nutrients typically have immunoenhancing properties, and recent advances in nutrition support involve studies designed to exploit the desirable biological properties of these nutrients. The term immunonutrition strictly implies that we are focusing on the effect of certain nutrients on aspects of the immune system. However, in reality immunonutrition also refers to studies that not only examine the function of lymphocytes and leucocytes, but which also study the influence of key nutrients on the acute-phase response, the inflammatory response and on gastrointestinal structure and function. The interest, therefore, is on the impact of immunonutrition on all aspects of host defence mechanisms in response to a catabolic stress. Major surgery evokes an acute-phase response, a transient immunosuppression and alterations in gastrointestinal function. Normal function is usually restored after a few days; however, in a subgroup of patients homeostasis may be lost and development of the systemic inflammatory response syndrome (SIRS) ensues. Results of recent clinical trials suggest that provision of immunomodulatory nutrients, including glutamine, arginine, n-3 polyunsaturated fatty acids and dietary nucleotides, may promote restoration of normal tissue function post-operatively and prevent the occurrence of SIRS.

scholarly journals The Importance of Psychoneuroimmunology for Social Workers

2018 ◽  
Vol 100 (1) ◽  
pp. 17-33
Author(s):  
Jill L. Littrell
Keyword(s):  
Immune System ◽  
Major Depression ◽  
Social Workers ◽  
Food Access ◽  
Psychotic Disorders ◽  
Stress Disorder ◽  
Food Preparation ◽  
And Behavior ◽  
The Impact ◽  
The Brain

A wealth of information regarding how the immune system can influence the brain and result in changes in mood and behavior has accumulated. Inflammation is a causal factor in some cases of major depression and psychotic disorders and predicts whether trauma will result in posttraumatic stress disorder (PTSD). Fortunately, studies in the area of psychoneuroimmunology have also suggested ways to decrease inflammation. Knowledge of this information is vital for social workers so that the impact of their interventions can be maximized. Moreover, for macropractice social workers, the information underscores the importance of access to nutritional food, access to safe places for exercise, and the time for food preparation and exercise, which should be considered as social justice issues.

The HPA and immune axes in stress: the involvement of the serotonergic system

2005 ◽  
Vol 20 (S3) ◽  
pp. S302-S306 ◽  
Author(s):  
B.E. Leonard
Keyword(s):  
Stress Response ◽  
Chronic Stress ◽  
Hpa Axis ◽  
Feedback Inhibition ◽  
Critical Role ◽  
Serotonergic System ◽  
Anxiety And Depression ◽  
Acute And Chronic Stress ◽  
The Impact ◽  
The Brain

AbstractThe impact of acute and chronic stress on the hypothalamic-pituitary-adrenal (HPA) axis is reviewed and evidence presented that corticotrophin releasing factor (CRF) is the stress neurotransmitter which plays an important role in the activation of the central sympathetic and serotonergic systems. The activity of CRF is expressed through specific receptors (CRF 1 and 2) that are antagonistic in their actions and widely distributed in the limbic regions of the brain, as well as in the hypothalamus, and on immune cells.The mechanism whereby chronic stress, via the CRF induced activation of the dorsal raphe nucleus, can induce a change in the serotonergic system, involves an increase in the 5HT2A and a decrease in the 5HT1A receptor mediated function. Such changes contribute to the onset of anxiety and depression. In addition, the hypersecretion of glucocorticoids that is associated with chronic stress and depression desensitises the central glucocorticoid receptors to the negative feedback inhibition of the HPA axis. This indirectly results in the further activation of the HPA axis.The rise in pro-inflammatory cytokines that usually accompanies the chronic stress response results in a further stimulation of the HPA axis thereby adding to the stress response. While CRF would appear to play a pivotal role, evidence is provided that simultaneous changes in the serotonergic and noradrenergic systems, combined with the activation of peripheral and central macrophages that increase the pro-inflammatory cytokine concentrations in the brain and blood, also play a critical role in predisposing to anxiety and depression. Neurodegenerative changes in the brain that frequently occur in the elderly patient with major depression, could result from the activation of indoleaminedioxygenase (IDO), a widely distributed enzyme that converts tryptophan via the kynenine pathway to for the neurotoxic end product quinolinic acid.

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