Stress and the Gut-Brain Axis: Implications for Cancer, Inflammation and Sepsis

Moughnyeh, Mohamad M.; Brawner, Kyle M.; Kennedy, Bethany A.; Yeramilli, Venkata A.; Udayakumar, Neha; Graham, Jessica A.; Martin, Colin

doi:10.1016/j.jss.2021.02.055

Cited by 10 publications

(10 citation statements)

References 100 publications

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“…Inflammatory Oxidative Medicine and Cellular Longevity cytokines such as IL-1β bind to IL-1β or prostaglandin E2 receptor in vagal fibers and increase vagal activity, which at last affects the nucleus tractus solitarius (NTS) by glutamate. The catecholaminergic neurons of the NTS project to different nuclei and cause sickness behaviors [66][67][68]. Neurotransmitters and neuromodulators derived from bacteria, gamma-aminobutyric acid, noradrenalin, serotonin, dopamine, and acetylcholine could change the state of brain by activating the vagus nerve [69].…”

Section: Activation Signals Of Neuroinflammationmentioning

confidence: 99%

Sepsis-Induced Brain Dysfunction: Pathogenesis, Diagnosis, and Treatment

Pan

Wang

et al. 2022

Oxidative Medicine and Cellular Longevity

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Dysregulated host response to infection, which cause life-threatening organ dysfunction, was defined as sepsis. Sepsis can cause acute and long-term brain dysfunction, namely, sepsis-associated encephalopathy (SAE) and cognitive impairment. SAE refers to changes in consciousness without direct evidence of central nervous system infection. It is highly prevalent and may cause poor outcomes in sepsis patients. Cognitive impairment seriously affects the life quality of sepsis patients and increases the medical burden. The pathogenesis of sepsis-induced brain dysfunction is mainly characterized by the interaction of systemic inflammation, blood-brain barrier (BBB) dysfunction, neuroinflammation, microcirculation dysfunction, and brain dysfunction. Currently, the diagnosis of sepsis-induced brain dysfunction is based on clinical manifestation of altered consciousness along with neuropathological examination, and the treatment is mainly involves controlling sepsis. Although treatments for sepsis-induced brain dysfunction have been tested in animals, clinical treat sepsis-induced brain dysfunction is still difficult. Therefore, we review the underlying mechanisms of sepsis-induced brain injury, which mainly focus on the influence of systemic inflammation on BBB, neuroinflammation, brain microcirculation, and the brain function, which want to bring new mechanism-based directions for future basic and clinical research aimed at preventing or ameliorating brain dysfunction.

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Section: Activation Signals Of Neuroinflammationmentioning

confidence: 99%

Sepsis-Induced Brain Dysfunction: Pathogenesis, Diagnosis, and Treatment

Pan

Wang

et al. 2022

Oxidative Medicine and Cellular Longevity

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“…The microbiota–gut–brain axis (MGBA) is a complex bidirectional communication system that integrates endocrine, immunological, and direct or indirect neural signalling pathways between the CNS, ENS, and the gut microbiota (Margolis et al, 2021). This axis can affect an organism at multiple levels, from modulating behaviour and influencing how and with whom, humans interact (Montiel‐Castro et al, 2013), to regulating mood, cognition, pain, obesity, cancer, and inflammatory and autoimmune diseases (Burokas et al, 2015; Margolis et al, 2021; Moughnyeh et al, 2021; Ting‐Ye et al, 2022). Thus, there is growing interest into the local and systemic effects this communication pathway has on host health and burden of disease.…”

Section: The Gi Tract and Gut Microbiomementioning

confidence: 99%

“…HPA axis dysregulation is associated with altered gut microbiome composition, affecting the neuroendocrine system and manifesting as anxiety‐like behaviour (Huo et al, 2017). Conversely, chronic exposure to stress can also activate the HPA axis, altering gut microbiota composition, and increasing peripheral inflammation (Moughnyeh et al, 2021). There is also evidence that neuroinflammation and neuroendocrine dysregulation may be involved in the pathogenesis of autism spectrum disorder, where patients present concomitantly with GI symptoms (Petra et al, 2015).…”

Section: The Gi Tract and Gut Microbiomementioning

confidence: 99%

The role of the microbiota–gut–brain axis in long‐term neurodegenerative processes following traumatic brain injury

Chiu

Anderton

2022

Eur J of Neuroscience

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“…T regs and ENS constitute a regulatory circuit in which microbial signals regulate neuronal density and activation, thereby regulating T regs generation and immune tolerance in the gut ( 120 ). The immune signals following sepsis or altered gut composition can cause the brain to respond to a perceived threat of infection and trigger an inflammatory response ( 123 ). Patients with sepsis, experience ectopic intestinal flora caused by acute stress, while survivors also experience chronic stress-induced depression and anxiety initiation mediated by gut-brain-axis immunity.…”

Section: T Regs -Related Therapeutic Potential In Saementioning

confidence: 99%

“…Patients with sepsis, experience ectopic intestinal flora caused by acute stress, while survivors also experience chronic stress-induced depression and anxiety initiation mediated by gut-brain-axis immunity. The gut-brainmicrobe axis is a promising therapeutic target for stressinduced behavioral injury, as it modulates both the peripheral and cerebral immune landscapes (121)(122)(123). The combination of probiotics and prebiotics promotes behavioral resilience to chronic stress by normalizing the gut microbiome and promoting T regs expansion, an impact reflecting behavioral responses better than neuroinflammation in limbic regions of brain.…”

Section: Regulating the Gut-brain Axismentioning

confidence: 99%

Insight Into Regulatory T Cells in Sepsis-Associated Encephalopathy

et al. 2022

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Sepsis-associated encephalopathy (SAE) is a diffuse central nervous system (CNS) dysfunction during sepsis, and is associated with increased mortality and poor outcomes in septic patients. Despite the high incidence and clinical relevance, the exact mechanisms driving SAE pathogenesis are not yet fully understood, and no specific therapeutic strategies are available. Regulatory T cells (Tregs) have a role in SAE pathogenesis, thought to be related with alleviation of sepsis-induced hyper-inflammation and immune responses, promotion of T helper (Th) 2 cells functional shift, neuroinflammation resolution, improvement of the blood-brain barrier (BBB) function, among others. Moreover, in a clinical point of view, these cells have the potential value of improving neurological and psychiatric/mental symptoms in SAE patients. This review aims to provide a general overview of SAE from its initial clinical presentation to long-term cognitive impairment and summarizes the main features of its pathogenesis. Additionally, a detailed overview on the main mechanisms by which Tregs may impact SAE pathogenesis is given. Finally, and considering that Tregs may be a novel target for immunomodulatory intervention in SAE, different therapeutic options, aiming to boost peripheral and brain infiltration of Tregs, are discussed.

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Stress and the Gut-Brain Axis: Implications for Cancer, Inflammation and Sepsis

Cited by 10 publications

References 100 publications

Sepsis-Induced Brain Dysfunction: Pathogenesis, Diagnosis, and Treatment

Sepsis-Induced Brain Dysfunction: Pathogenesis, Diagnosis, and Treatment

The role of the microbiota–gut–brain axis in long‐term neurodegenerative processes following traumatic brain injury

Insight Into Regulatory T Cells in Sepsis-Associated Encephalopathy

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