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Article ; Online: Stress in the microbiome-immune crosstalk.

Beurel, Eléonore

2024 Volume 16, Issue 1, Page(s) 2327409

Abstract: The gut microbiota exerts a mutualistic interaction with the host in a fragile ecosystem and the host intestinal, neural, and immune cells. Perturbations of the gastrointestinal track composition after stress have profound consequences on the central ... ...

Abstract	The gut microbiota exerts a mutualistic interaction with the host in a fragile ecosystem and the host intestinal, neural, and immune cells. Perturbations of the gastrointestinal track composition after stress have profound consequences on the central nervous system and the immune system. Reciprocally, brain signals after stress affect the gut microbiota highlighting the bidirectional communication between the brain and the gut. Here, we focus on the potential role of inflammation in mediating stress-induced gut-brain changes and discuss the impact of several immune cells and inflammatory molecules of the gut-brain dialogue after stress. Understanding the impact of microbial changes on the immune system after stress might provide new avenues for therapy.
MeSH term(s)	Humans ; Gastrointestinal Microbiome/physiology ; Microbiota ; Brain/physiology ; Nervous System ; Inflammation
Language	English
Publishing date	2024-03-15
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2575755-6
ISSN	1949-0984 ; 1949-0984
ISSN (online)	1949-0984
ISSN	1949-0984
DOI	10.1080/19490976.2024.2327409
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Article ; Online: Inflammatory and neurodegenerative pathophysiology implicated in postpartum depression.

Worthen, Ryan J / Beurel, Eleonore

Neurobiology of disease

2022 Volume 165, Page(s) 105646

Abstract: Postpartum depression (PPD) is the most common psychiatric complication associated with pregnancy and childbirth with debilitating symptoms that negatively impact the quality of life of the mother as well as inflict potentially long-lasting developmental ...

Abstract	Postpartum depression (PPD) is the most common psychiatric complication associated with pregnancy and childbirth with debilitating symptoms that negatively impact the quality of life of the mother as well as inflict potentially long-lasting developmental impairments to the child. Much of the theoretical pathophysiology put forth to explain the emergence of PPD overlaps with that of major depressive disorder (MDD) and, although not conventionally described in such terms, can be seen as neurodegenerative in nature. Framing the disorder from the perspective of the well-established inflammatory theory of depression, symptoms are thought to be driven by dysregulation, and subsequent hyperactivation of the body's immune response to stress. Compounded by physiological stressors such as drastic fluctuations in hormone signaling, physical and psychosocial stressors placed upon new mothers lay bare a number of significant vulnerabilities, or points of potential failure, in systems critical for maintaining healthy brain function. The inability to compensate or properly adapt to meet the changing demands placed upon these systems has the potential to damage neurons, hinder neuronal growth and repair, and disrupt neuronal circuit integrity such that essential functional outputs like mood and cognition are altered. The impact of this deterioration in brain function, which includes depressive symptoms, extends to the child who relies on the mother for critical life-sustaining care as well as important cognitive stimulation, accentuating the need for further research.
MeSH term(s)	Child ; Depression/psychology ; Depression, Postpartum/diagnosis ; Depression, Postpartum/psychology ; Depressive Disorder, Major ; Female ; Humans ; Pregnancy ; Quality of Life ; Risk Factors
Language	English
Publishing date	2022-01-29
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	1211786-9
ISSN	1095-953X ; 0969-9961
ISSN (online)	1095-953X
ISSN	0969-9961
DOI	10.1016/j.nbd.2022.105646
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Article ; Online: Stress promotes the infiltration of peripheral immune cells to the brain.

Medina-Rodriguez, Eva M / Han, Dongmei / Lowell, Jeffrey / Beurel, Eléonore

Brain, behavior, and immunity

2023 Volume 111, Page(s) 412–423

Abstract: Immune cells and the brain have a privileged interaction. Here, we report changes in the hippocampal immune microenvironment at the single cell level after stress, uncovering the tight orchestration of immune cell infiltration into the hippocampus after ... ...

Abstract	Immune cells and the brain have a privileged interaction. Here, we report changes in the hippocampal immune microenvironment at the single cell level after stress, uncovering the tight orchestration of immune cell infiltration into the hippocampus after stress to maintain homeostasis. We show the distribution of several immune cell types in the hippocampus associated with their susceptibility or resilience to the learned helplessness paradigm in a sex- and microbiota-dependent manner using single-cell RNA sequencing and bioinformatic tools, flow cytometry, and immunofluorescence. We uncovered the presence of tissue-resident memory T cells that accumulate over time in the hippocampus of learned helpless mice, and the presence of CD74-expressing myeloid cells. These cells were found by a knockdown approach to be critical to induce resilience to learned helplessness. Altogether, these findings provide a novel overview of the neuro-immune repertoire and its impact on the landscape of the hippocampus after learned helplessness.
MeSH term(s)	Mice ; Animals ; Brain ; Hippocampus/metabolism ; Helplessness, Learned ; Stress, Psychological/metabolism
Language	English
Publishing date	2023-05-09
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	639219-2
ISSN	1090-2139 ; 0889-1591
ISSN (online)	1090-2139
ISSN	0889-1591
DOI	10.1016/j.bbi.2023.05.003
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Zs.A 2276: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Blood brain barrier and inflammation in depression.

Medina-Rodriguez, Eva M / Beurel, Eléonore

Neurobiology of disease

2022 Volume 175, Page(s) 105926

Abstract: The blood brain barrier (BBB) is a vital structure to protect the brain, tightly filtering the passage of nutrients and molecules from the blood to the brain. This is critical for maintaining the proper functioning of the brain, and any disruption in the ...

Abstract	The blood brain barrier (BBB) is a vital structure to protect the brain, tightly filtering the passage of nutrients and molecules from the blood to the brain. This is critical for maintaining the proper functioning of the brain, and any disruption in the BBB has detrimental consequences often leading to diseases. It is not clear whether disruption of the BBB occurs first in depression or is the consequence of the disease, however disruption of the BBB has been observed in depressed patients and evidence points to the role of important culprits in depression, stress and inflammation in disrupting the integrity of the BBB. The mechanisms whereby stress, and inflammation affect the BBB remain to be fully understood. Yet, the role of cytokines in regulating tight junction protein expression seems crucial. Altogether, the findings in depression suggest that acting at the BBB level might provide therapeutic benefit in depression.
MeSH term(s)	Humans ; Blood-Brain Barrier/metabolism ; Depression ; Inflammation/metabolism ; Biological Transport ; Brain/metabolism
Language	English
Publishing date	2022-11-12
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1211786-9
ISSN	1095-953X ; 0969-9961
ISSN (online)	1095-953X
ISSN	0969-9961
DOI	10.1016/j.nbd.2022.105926
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Article ; Online: Targeting the Adaptive Immune System in Depression: Focus on T Helper 17 Cells.

Beurel, Eléonore / Medina-Rodriguez, Eva M / Jope, Richard S

Pharmacological reviews

2022 Volume 74, Issue 2, Page(s) 373–386

Abstract: There is a vital need to understand mechanisms contributing to susceptibility to depression to improve treatments for the 11% of Americans who currently suffer from this debilitating disease. The adaptive immune system, comprising T and B cells, has ... ...

Abstract	There is a vital need to understand mechanisms contributing to susceptibility to depression to improve treatments for the 11% of Americans who currently suffer from this debilitating disease. The adaptive immune system, comprising T and B cells, has emerged as a potential contributor to depression, as demonstrated in the context of lymphopenic mice. Overall, patients with depression have reduced circulating T and regulatory B cells, "immunosuppressed" T cells, and alterations in the relative abundance of T cell subtypes. T helper (Th) cells have the capacity to differentiate to various lineages depending on the cytokine environment, antigen stimulation, and costimulation. Regulatory T cells are decreased, and the Th1/Th2 ratio and the Th17 cells are increased in patients with depression. Evidence for changes in each Th lineage has been reported to some extent in patients with depression. However, the evidence is strongest for the association of depression with changes in Th17 cells. Th17 cells produce the inflammatory cytokine interleukin (IL)-17A, and the discovery of Th17 cell involvement in depression evolved from the well established link that IL-6, which is required for Th17 cell differentiation, contributes to the onset, and possibly maintenance, of depression. One intriguing action of Th17 cells is their participation in the gut-brain axis to mediate stress responses. Although the mechanisms of action of Th17 cells in depression remain unclear, neutralization of IL-17A by anti-IL-17A antibodies, blocking stress-induced production, or release of gut Th17 cells represent feasible therapeutic approaches and might provide a new avenue to improve depression symptoms. SIGNIFICANCE STATEMENT: Th17 cells appear as a promising therapeutic target for depression, for which efficacious therapeutic options are limited. The use of neutralizing antibodies targeting Th17 cells has provided encouraging results in depressed patients with comorbid autoimmune diseases.
MeSH term(s)	Animals ; Cytokines ; Depression ; Humans ; Mice ; T-Lymphocytes, Regulatory ; Th17 Cells
Chemical Substances	Cytokines
Language	English
Publishing date	2022-03-17
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	209898-2
ISSN	1521-0081 ; 0031-6997
ISSN (online)	1521-0081
ISSN	0031-6997
DOI	10.1124/pharmrev.120.000256
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Article ; Online: Th17 cells sense microbiome to promote depressive-like behaviors.

Medina-Rodriguez, Eva M / Watson, Jowan / Reyes, Juliana / Trivedi, Madhukar / Beurel, Eléonore

Microbiome

2023 Volume 11, Issue 1, Page(s) 92

Abstract: Background: Microbiome alterations have been associated with depression, and fecal transfer of depressed patients' microbiomes is sufficient to enhance despair behaviors in rodents. Yet little is known about the potential mechanisms, whereby microbes ... ...

Abstract	Background: Microbiome alterations have been associated with depression, and fecal transfer of depressed patients' microbiomes is sufficient to enhance despair behaviors in rodents. Yet little is known about the potential mechanisms, whereby microbes modulate depressive-like behaviors. Results: In this study, we showed that certain bacteria known to induce Th17 cells are increased in depressed patients and mice exhibiting learned helplessness. Fecal transfers of human depressed patients' microbiomes into germ-free-like mice were sufficient to decrease sociability and increased susceptibility to the learned helplessness paradigm, confirming that the microbiome is sufficient to confer depressive-like behaviors. This microbial effect was dependent on the presence of Th17 cells in the recipient, as germ-free-like recipient mice deficient in Th17 cells were resistant to the behavioral changes induced by the microbiome of depressed patients. Conclusion: Altogether, these findings suggest a crucial role of the microbiome/Th17 cell axis in regulating depressive-like behaviors. Video Abstract.
MeSH term(s)	Humans ; Mice ; Animals ; Th17 Cells ; Gastrointestinal Microbiome/physiology ; Depression/microbiology ; Microbiota ; Feces
Language	English
Publishing date	2023-04-28
Publishing country	England
Document type	Video-Audio Media ; Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2697425-3
ISSN	2049-2618 ; 2049-2618
ISSN (online)	2049-2618
ISSN	2049-2618
DOI	10.1186/s40168-022-01428-3
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Article ; Online: Stress, inflammation, microbiome and depression.

Medina-Rodriguez, Eva M / Cruz, Alyssa A / De Abreu, Julia Cavati / Beurel, Eléonore

Pharmacology, biochemistry, and behavior

2023 Volume 227-228, Page(s) 173561

Abstract: Psychiatric disorders are mental illnesses involving changes in mood, cognition and behavior. Their prevalence has rapidly increased in the last decades. One of the most prevalent psychiatric disorders is major depressive disorder (MDD), a debilitating ... ...

Abstract	Psychiatric disorders are mental illnesses involving changes in mood, cognition and behavior. Their prevalence has rapidly increased in the last decades. One of the most prevalent psychiatric disorders is major depressive disorder (MDD), a debilitating disease lacking efficient treatments. Increasing evidence shows that microbial and immunological changes contribute to the pathophysiology of depression and both are modulated by stress. This bidirectional relationship constitutes the brain-gut axis involving various neuroendocrine, immunological, neuroenterocrine and autonomic pathways. The present review covers the most recent findings on the relationships between stress, the gut microbiome and the inflammatory response and their contribution to depression.
MeSH term(s)	Humans ; Depression/metabolism ; Depressive Disorder, Major/metabolism ; Gastrointestinal Microbiome/physiology ; Affect ; Inflammation/metabolism ; Brain/metabolism
Language	English
Publishing date	2023-05-05
Publishing country	United States
Document type	Review ; Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	191042-5
ISSN	1873-5177 ; 0091-3057
ISSN (online)	1873-5177
ISSN	0091-3057
DOI	10.1016/j.pbb.2023.173561
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Zs.A 1060: Show issues

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Article ; Online: Regulation of inflammation and T cells by glycogen synthase kinase-3: links to mood disorders.

Beurel, Eleonore

Neuroimmunomodulation

2014 Volume 21, Issue 2-3, Page(s) 140–144

Abstract: Accumulative evidence shows a role of the immune system in susceptibility to depression. Proinflammatory cytokines have been shown to be involved in the induction of depressive behavior both in humans and mice, opening a new avenue of therapeutic ... ...

Abstract	Accumulative evidence shows a role of the immune system in susceptibility to depression. Proinflammatory cytokines have been shown to be involved in the induction of depressive behavior both in humans and mice, opening a new avenue of therapeutic strategy. Because glycogen synthase kinase-3 (GSK3) was recently identified to be controlling the production of proinflammatory cytokines, and GSK3 has been shown to be implicated in mood disorders for many years, it has been proposed that the proinflammatory action of GSK3 could be responsible for the increased susceptibility to depressive behavior. Moreover, besides regulating cytokines, GSK3 also promotes differentiation of proinflammatory subtypes of Th cells, which are sufficient to induce depressive behavior in mice. Although the clear involvement of the immune system during depressive behavior still needs to be firmly demonstrated, there is growing evidence for the involvement of inflammation in the induction of depressive behavior.
MeSH term(s)	Animals ; Glycogen Synthase Kinase 3/immunology ; Humans ; Inflammation/enzymology ; Inflammation/immunology ; Mood Disorders/enzymology ; Mood Disorders/immunology ; T-Lymphocytes/enzymology ; T-Lymphocytes/immunology
Chemical Substances	Glycogen Synthase Kinase 3 (EC 2.7.11.26)
Language	English
Publishing date	2014-02-14
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	1184368-8
ISSN	1423-0216 ; 1021-7401
ISSN (online)	1423-0216
ISSN	1021-7401
DOI	10.1159/000356550
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Article ; Online: The Bidirectional Relationship of Depression and Inflammation: Double Trouble.

Beurel, Eléonore / Toups, Marisa / Nemeroff, Charles B

Neuron

2020 Volume 107, Issue 2, Page(s) 234–256

Abstract: Depression represents the number one cause of disability worldwide and is often fatal. Inflammatory processes have been implicated in the pathophysiology of depression. It is now well established that dysregulation of both the innate and adaptive immune ... ...

Abstract	Depression represents the number one cause of disability worldwide and is often fatal. Inflammatory processes have been implicated in the pathophysiology of depression. It is now well established that dysregulation of both the innate and adaptive immune systems occur in depressed patients and hinder favorable prognosis, including antidepressant responses. In this review, we describe how the immune system regulates mood and the potential causes of the dysregulated inflammatory responses in depressed patients. However, the proportion of never-treated major depressive disorder (MDD) patients who exhibit inflammation remains to be clarified, as the heterogeneity in inflammation findings may stem in part from examining MDD patients with varied interventions. Inflammation is likely a critical disease modifier, promoting susceptibility to depression. Controlling inflammation might provide an overall therapeutic benefit, regardless of whether it is secondary to early life trauma, a more acute stress response, microbiome alterations, a genetic diathesis, or a combination of these and other factors.
MeSH term(s)	Affect ; Antidepressive Agents/therapeutic use ; Depression/immunology ; Depression/physiopathology ; Depression/psychology ; Depressive Disorder, Major/immunology ; Depressive Disorder, Major/physiopathology ; Depressive Disorder, Major/psychology ; Humans ; Immune System/physiopathology ; Inflammation/immunology ; Inflammation/physiopathology ; Inflammation/psychology
Chemical Substances	Antidepressive Agents
Language	English
Publishing date	2020-06-17
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	808167-0
ISSN	1097-4199 ; 0896-6273
ISSN (online)	1097-4199
ISSN	0896-6273
DOI	10.1016/j.neuron.2020.06.002
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Zs.A 2496: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 92: Show issues

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Article ; Online: Regulation by glycogen synthase kinase-3 of inflammation and T cells in CNS diseases.

Beurel, Eléonore

Frontiers in molecular neuroscience

2011 Volume 4, Page(s) 18

Abstract: Elevated markers of neuroinflammation have been found to be associated with many psychiatric and neurodegenerative diseases, such as mood disorders, Alzheimer's disease, and multiple sclerosis (MS). Since neuroinflammation is thought to contribute to the ...

Abstract	Elevated markers of neuroinflammation have been found to be associated with many psychiatric and neurodegenerative diseases, such as mood disorders, Alzheimer's disease, and multiple sclerosis (MS). Since neuroinflammation is thought to contribute to the pathophysiology of these diseases and to impair responses to therapeutic interventions and recovery, it is important to identify mechanisms that regulate neuroinflammation and potential targets for controlling neuroinflammation. Recent findings have demonstrated that glycogen synthase kinase-3 (GSK3) is an important regulator of both the innate and adaptive immune systems' contributions to inflammation. Studies of the innate immune system have shown that inhibitors of GSK3 profoundly alter the repertoire of cytokines that are produced both by peripheral and central cells, reducing pro-inflammatory cytokines, and increasing anti-inflammatory cytokines. Furthermore, inhibitors of GSK3 promote tolerance to inflammatory stimuli, reducing inflammatory cytokine production upon repeated exposure. Studies of the adaptive immune system have shown that GSK3 regulates the production of cytokines by T cells and the differentiation of T cells to subtypes, particularly Th17 cells. Regulation of transcription factors by GSK3 appears to play a prominent role in its regulation of immune responses, including of NF-κB, cyclic AMP response element binding protein, and signal transducer and activator of transcription-3. Invivo studies have shown that GSK3 inhibitors ameliorate clinical symptoms of both peripheral and central inflammatory diseases, particularly experimental autoimmune encephalomyelitis, the animal model of MS. Therefore, the development and application of GSK3 inhibitors may provide a new therapeutic strategy to reduce neuroinflammation associated with many central nervous system diseases.
Language	English
Publishing date	2011-08-31
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2452967-9
ISSN	1662-5099 ; 1662-5099
ISSN (online)	1662-5099
ISSN	1662-5099
DOI	10.3389/fnmol.2011.00018
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