Gut Inflammation: More Than a Peripheral Annoyance

Gray, Marcus A.; Holtmann, Gerald

doi:10.1007/s10620-017-4587-x

Cited by 3 publications

(2 citation statements)

References 11 publications

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“…Furthermore, the generally heightened threat expectations due to the chronic immunological priming of microglia by a lingering virus increase the body's readiness to infection, maintaining the individual in an energy-intensive state of alertness ( 16 , 53 ). Consistent activation of immunological responses may cause chronic inflammation and microbial dysbiosis, reinforcing the negative cycle of suboptimal organismic functioning and maintaining the individual in an anxious state to the point where the anxiety is internalized and becomes a trait ( 16 , 54 , 55 ).…”

Section: The Dmn: Persistent Infection Aversive Learning and Anxietymentioning

confidence: 99%

SARS-CoV-2, Trait Anxiety, and the Microbiome

et al. 2021

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During the COVID-19 pandemic, research on the relationships between the virus and its human host has become fundamental to understand this pathology and its effects. Attaining this profound understanding is critical for the effective containment and treatment of infections caused by the virus. In this review, we present some possible mechanisms by which psychopathological symptoms emerge following viral infections of the central nervous system (CNS). These proposed mechanisms are based on microbial communication and the induced priming of microglial antibody activation within the CNS through Toll-like receptor signaling. In this process, chronic microglial activation causes increased glutamate release in virally-altered, high-density neuronal structures, thereby modulating cognitive networks and information integration processes. This modulation, in turn, we suggest, affects the accuracy of sensory integration and connectivity of major control networks, such as the default mode network. The chronic activation of immunological responses and neurochemical shifts toward an elevated glutamate/gamma-aminobutyric acid ratio lead to negative reinforcement learning and suboptimal organismic functioning, for example, maintaining the body in an anxious state, which can later become internalized as trait anxiety. Therefore, we hypothesize that the homeostatic relationship between host, microbiome, and virome, would be decisive in determining the efficiency of subsequent immunological responses, disease susceptibility, and long-term psychopathological effects of diseases that impact the CNS, such as the COVID-19.

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Section: The Dmn: Persistent Infection Aversive Learning and Anxietymentioning

confidence: 99%

SARS-CoV-2, Trait Anxiety, and the Microbiome

et al. 2021

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“…Therefore, an increase in the production of antibodies, free reactive compounds such as histamine, and down-regulation of inactivating enzymes such as diamine oxidase, may eventually occur [ 32 ]. Inflammation of the gastrointestinal tract affects microbial symbiosis, and may induce long-term neuromodulatory changes through microbial signaling [ 10 , 35 , 37 , 38 ]. The resulting unfavorable endocrine and neurochemical conditions may become chronic.…”

Section: Microbial Dysbiosis and The Emergence Of Anxietymentioning

confidence: 99%

Interoception, Trait Anxiety, and the Gut Microbiome: A Cognitive and Physiological Model

et al. 2021

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Trait anxiety is characterized as a constant and often subliminal state that persists during daily life. Interoception is the perception of internal states and sensations, including from the autonomic nervous system. This review aims to develop a predictive model to explain the emergence, manifestations, and maintenance of trait anxiety. The model begins with the assumption that anxiety states arise from active interoceptive inference. The subsequent activation of autonomic responses results from aversive sensory encounters. A cognitive model is proposed for trait anxiety that includes the aversive sensory components from interoception, exteroception, and proprioception. A further component of the hypothesis is that repeated exposure to subliminal anxiety-evoking sensory elements can lead to an overgeneralization of this response to other inputs that are generally non-aversive. Increased uncertainty may result when predicting the sensory environment, resulting in arbitrary interoceptive anxiety responses that may be due to unjustifiable causes. Arbitrary successful or unsuccessful matching of predictions and responses reduces the individual’s confidence to maintain the anxiety trait. In this review, the application of the proposed model is illustrated using gut microbial dysbiosis or imbalance of the gut microbiome.

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Altered brain structural connectivity in patients with longstanding gut inflammation is correlated with psychological symptoms and disease duration

Turkiewicz

Bhatt

Wang

et al. 2021

NeuroImage: Clinical

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Highlights IBS and Ulcerative Colitis (UC) patients have changes in brain network organization. Changes in brain network organization correlate with disease symptomatology. In UC, brain network organization changes correlate with disease duration. Chronic gut inflammation as well as pain have neuroplastic effects on the brain.

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Gut Inflammation: More Than a Peripheral Annoyance

Cited by 3 publications

References 11 publications

SARS-CoV-2, Trait Anxiety, and the Microbiome

SARS-CoV-2, Trait Anxiety, and the Microbiome

Interoception, Trait Anxiety, and the Gut Microbiome: A Cognitive and Physiological Model

Altered brain structural connectivity in patients with longstanding gut inflammation is correlated with psychological symptoms and disease duration

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