scholarly journals From Probiotics to Psychobiotics: Live Beneficial Bacteria Which Act on the Brain-Gut Axis

Nutrients ◽  
2019 ◽  
Vol 11 (4) ◽  
pp. 890 ◽  
Author(s):  
Luis G. Bermúdez-Humarán ◽  
Eva Salinas ◽  
Genaro G. Ortiz ◽  
Luis J. Ramirez-Jirano ◽  
J. Alejandro Morales ◽  
...  
Keyword(s):  
Nervous System ◽  
Immune System ◽  
Affective Disorders ◽  
Probiotic Bacteria ◽  
Cognitive Level ◽  
Beneficial Bacteria ◽  
Important Relationship ◽  
And Control ◽  
The Brain ◽  
Pituitary Adrenal Axis

There is an important relationship between probiotics, psychobiotics and cognitive and behavioral processes, which include neurological, metabolic, hormonal and immunological signaling pathways; the alteration in these systems may cause alterations in behavior (mood) and cognitive level (learning and memory). Psychobiotics have been considered key elements in affective disorders and the immune system, in addition to their effect encompassing the regulation of neuroimmune regulation and control axes (the hypothalamic-pituitary-adrenal axis or HPA, the sympathetic-adrenal-medullary axis or SAM and the inflammatory reflex) in diseases of the nervous system. The aim of this review is to summarize the recent findings about psychobiotics, the brain-gut axis and the immune system. The review focuses on a very new and interesting field that relates the microbiota of the intestine with diseases of the nervous system and its possible treatment, in neuroimmunomodulation area. Indeed, although probiotic bacteria will be concentrated after ingestion, mainly in the intestinal epithelium (where they provide the host with essential nutrients and modulation of the immune system), they may also produce neuroactive substances which act on the brain-gut axis.

scholarly journals Targeting the CCL2-CCR2 axis in depressive disorders

2021 ◽  
Author(s):  
Katarzyna Curzytek ◽  
Monika Leśkiewicz
Keyword(s):  
Nervous System ◽  
Immune System ◽  
Affective Disorders ◽  
Depressive Disorders ◽  
Brain Diseases ◽  
Receptor System ◽  
Proinflammatory Mediators ◽  
Pathological Conditions ◽  
The Central Nervous System ◽  
Abnormal Brain

AbstractSince affective disorders are considered to be underlain by the immune system malfunction, an important role in their pathophysiology is assigned to the proinflammatory mediators. Recently, chemokines, the group of chemotactic cytokines, have become a focus for basic and clinical scientists in the context of the development and treatment of brain diseases. Among them, chemokine CCL2 and its main receptor CCR2 have become candidate mediators of abnormal brain-immune system dialogue in depression. Besides the chemotactic activity, the CCL2-CCR2 axis is involved in various neurobiological processes, neurogenesis, neurotransmission, neuroinflammation, neurodegeneration, as well as neuroregeneration. Given the range of immunomodulatory possibilities that the CCL2-CCR2 pair can exert on the nervous system, its proinflammatory properties were initially thought to be a major contributor to the development of depressive disorders. However, further research suggests that the malfunctions of the nervous system are rather associated with impaired homeostatic properties manifested by the CCL2-CCR2 dyad dysfunctions. This review aims to present literature data on the action of the CCL2-CCR2 axis in the central nervous system under physiological and pathological conditions, as well as the contribution of this ligand-receptor system to the processes underlying affective disorders. Additionally, this article draws attention to the importance of the CCL2-CRR2 pathway as a potential pharmacological target with antidepressant potential.

Interleukin-1β and neurogenic control of blood pressure in normal rats and rats with chronic renal failure

2000 ◽  
Vol 279 (6) ◽  
pp. H2786-H2796 ◽  
Author(s):  
Shaohua Ye ◽  
Pantea Mozayeni ◽  
Michael Gamburd ◽  
Huiqin Zhong ◽  
Vito M. Campese
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Renal Failure ◽  
Nervous System ◽  
Chronic Renal Failure ◽  
Lateral Ventricle ◽  
Mrna Abundance ◽  
And Control ◽  
The Brain ◽  
Local Expression

Increased sympathetic nervous system (SNS) activity plays a role in the genesis of hypertension in rats with chronic renal failure (CRF). The rise in central SNS activity is mitigated by increased local expression of neuronal nitric oxide synthase (NOS) mRNA and NO2/NO3 production. Because interleukin (IL)-1β may activate nitric oxide in the brain, we have tested the hypothesis that IL-1β may modulate the activity of the SNS via regulation of the local expression of neuronal NOS (nNOS) in the brain of CRF and control rats. To this end, we first found that administration of IL-1β in the lateral ventricle of control and CRF rats decreased blood pressure and norepinephrine (NE) secretion from the posterior hypothalamus (PH) and increased NOS mRNA expression. Second, we observed that an acute or chronic injection of an IL-1β-specific antibody in the lateral ventricle raised blood pressure and NE secretion from the PH and decreased NOS mRNA abundance in the PH of control and CRF rats. Finally, we measured the IL-1β mRNA abundance in the PH, locus coeruleus, and paraventricular nuclei of CRF and control rats by RT-PCR and found it to be greater in CRF rats than in control rats. In conclusion, these studies have shown that IL-1β modulates the activity of the SNS in the central nervous system and that this modulation is mediated by increased local expression of nNOS mRNA.

Immune surveillance and tumors of the nervous system

1978 ◽  
Vol 49 (1) ◽  
pp. 84-92 ◽  
Author(s):  
Robert A. Morantz ◽  
William Shain ◽  
Humberto Cravioto
Keyword(s):  
Nervous System ◽  
Immune System ◽  
Surveillance System ◽  
Immune Surveillance ◽  
Tumor Formation ◽  
Pregnant Rats ◽  
Content Type ◽  
System Tumor ◽  
The Brain ◽  
Fine Print

✓ 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.

The Ouroboros of Inflammatory Signaling to the Brain for the Control of Neuroendocrine Function

2021 ◽  
Author(s):  
Georgia E. Hodes
Keyword(s):  
Nervous System ◽  
Immune System ◽  
Immune Regulation ◽  
The Body ◽  
Immune Disorders ◽  
Inflammatory Signaling ◽  
Late 20Th Century ◽  
Immune Systems ◽  
Neuroendocrine Function ◽  
The Brain

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.

scholarly journals Immune System in the Brain: A Modulatory Role on Dendritic Spine Morphophysiology?

2012 ◽  
Vol 2012 ◽  
pp. 1-7 ◽  
Author(s):  
Oscar Kurt Bitzer-Quintero ◽  
Ignacio González-Burgos
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Immune System ◽  
Dendritic Spines ◽  
Cell Lineage ◽  
Myeloid Cell ◽  
Brain Parenchyma ◽  
Immune Mediators ◽  
The Central Nervous System ◽  
The Brain

The central nervous system is closely linked to the immune system at several levels. The brain parenchyma is separated from the periphery by the blood brain barrier, which under normal conditions prevents the entry of mediators such as activated leukocytes, antibodies, complement factors, and cytokines. The myeloid cell lineage plays a crucial role in the development of immune responses at the central level, and it comprises two main subtypes: (1) resident microglia, distributed throughout the brain parenchyma; (2) perivascular macrophages located in the brain capillaries of the basal lamina and the choroid plexus. In addition, astrocytes, oligodendrocytes, endothelial cells, and, to a lesser extent, neurons are implicated in the immune response in the central nervous system. By modulating synaptogenesis, microglia are most specifically involved in restoring neuronal connectivity following injury. These cells release immune mediators, such as cytokines, that modulate synaptic transmission and that alter the morphology of dendritic spines during the inflammatory process following injury. Thus, the expression and release of immune mediators in the brain parenchyma are closely linked to plastic morphophysiological changes in neuronal dendritic spines. Based on these observations, it has been proposed that these immune mediators are also implicated in learning and memory processes.

scholarly journals Standarization of a Protocol of Immunohistochemistry for the Detection of Brain Microglia in Wistar Rats

2017 ◽  
Vol 19 (3) ◽  
pp. 45
Author(s):  
Karol Ramírez Chan DDS, MSc, PhD ◽  
Jaime Jaime Fornaguera-Trías PhD
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Immune System ◽  
Wistar Rats ◽  
Secondary Antibody ◽  
Research Activity ◽  
The Central Nervous System ◽  
Near Future ◽  
The Brain ◽  
Microglia Morphology

Objective: Standardize a protocol of immunohistochemistry that has been widely used in C57BL/6J mice to identify microglia of the central nervous system in Wistar rats.  Materials and Methods: This research activity was carried out in two parts. In the first part, a protocol of immunohistochemistry was implemented to identify microglia in the central nervous system of 6 Wistar rats. A primary antibody with reactivity to rat and a specific secondary antibody to the primary were used. Once the protocol was established in rats' brains, an immunological challenge was produced with the intraperitoneal application of lipopolysaccharide in 2 Wistar rats, in order to evidence the changes in microglia morphology.  Results and Discussion: We demonstrate that without making major modifications to the original protocol, it can also be used to identify microglia in adult Wistar rats. In the near future, this immunostaining protocol will be applied to elucidate the bidirectional interaction between the brain and the immune system, under homeostatic conditions and different physiological and pathological stimuli.

Microbiota-immune interactions: from gut to brain

2020 ◽  
Vol 7 (1) ◽  
pp. 1-23 ◽  
Author(s):  
Eloisa Salvo-Romero ◽  
Patricia Stokes ◽  
Mélanie G. Gareau
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Immune System ◽  
Gut Microbiota ◽  
Brain Development ◽  
Immune Cells ◽  
Autism Spectrum ◽  
Immune System Development ◽  
And Function ◽  
The Brain

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.

scholarly journals Oligodendrocyte lineage cells and depression

2020 ◽  
Author(s):  
Butian Zhou ◽  
Zhongqun Zhu ◽  
Bruce R. Ransom ◽  
Xiaoping Tong
Keyword(s):  
Central Nervous System ◽  
Mental Illness ◽  
Nervous System ◽  
Immune System ◽  
Oligodendrocyte Progenitor Cells ◽  
Myelin Sheaths ◽  
Novel Strategy ◽  
Environmental Milieu ◽  
Pituitary Adrenal Axis ◽  
Shed Light

Abstract Depression is a common mental illness, affecting more than 300 million people worldwide. Decades of investigation have yielded symptomatic therapies for this disabling condition but have not led to a consensus about its pathogenesis. There are data to support several different theories of causation, including the monoamine hypothesis, hypothalamic–pituitary–adrenal axis changes, inflammation and immune system alterations, abnormalities of neurogenesis and a conducive environmental milieu. Research in these areas and others has greatly advanced the current understanding of depression; however, there are other, less widely known theories of pathogenesis. Oligodendrocyte lineage cells, including oligodendrocyte progenitor cells and mature oligodendrocytes, have numerous important functions, which include forming myelin sheaths that enwrap central nervous system axons, supporting axons metabolically, and mediating certain forms of neuroplasticity. These specialized glial cells have been implicated in psychiatric disorders such as depression. In this review, we summarize recent findings that shed light on how oligodendrocyte lineage cells might participate in the pathogenesis of depression, and we discuss new approaches for targeting these cells as a novel strategy to treat depression.

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