The Interface between Inflammatory Bowel Disease, Neuroinflammation, and Neurological Disorders

Hey, Grace; Vedam‐Mai, Vinata; Beke, Matthew; Amaris, Manuel A.; Ramirez‐Zamora, Adolfo

doi:10.1055/s-0043-1771467

Cited by 4 publications

(11 citation statements)

References 129 publications

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“…Chronic inflammation, damage to the gut mucosa, and immune system dysregulation in IBD can lead to structural and functional alterations within the ENS, therefore potentially altering communication through the GBA (Figure 1B) [23][24][25]. Myenteric plexitis has been reported in a majority of CD (75%) and UC (56%) cases [26].…”

Section: Enteric Nervous System Alterations In Ibdmentioning

confidence: 99%

Enteric Nervous System Alterations in Inflammatory Bowel Disease: Perspectives and Implications

Suman

2024

Gastrointestinal Disorders

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The enteric nervous system (ENS), consisting of neurons and glial cells, is situated along the gastrointestinal (GI) tract’s wall and plays a crucial role in coordinating digestive processes. Recent research suggests that the optimal functioning of the GI system relies on intricate connections between the ENS, the intestinal epithelium, the immune system, the intestinal microbiome, and the central nervous system (CNS). Inflammatory bowel disease (IBD) encompasses a group of chronic inflammatory disorders, such as Crohn’s disease (CD) and ulcerative colitis (UC), characterized by recurring inflammation and damage to the GI tract. This review explores emerging research in the dynamic field of IBD and sheds light on the potential role of ENS alterations in both the etiology and management of IBD. Specifically, we delve into IBD-induced enteric glial cell (EGC) activation and its implications for persistent enteric gliosis, elucidating how this activation disrupts GI function through alterations in the gut–brain axis (GBA). Additionally, we examine IBD-associated ENS alterations, focusing on EGC senescence and the acquisition of the senescence-associated secretory phenotype (SASP). We highlight the pivotal role of these changes in persistent GI inflammation and the recurrence of IBD. Finally, we discuss potential therapeutic interventions involving senotherapeutic agents, providing insights into potential avenues for managing IBD by targeting ENS-related mechanisms. This approach might represent a potential alternative to managing IBD and advance treatment of this multifaceted disease.

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Section: Enteric Nervous System Alterations In Ibdmentioning

confidence: 99%

Enteric Nervous System Alterations in Inflammatory Bowel Disease: Perspectives and Implications

Suman

2024

Gastrointestinal Disorders

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“…However, a meta-analysis of cohort studies revealed an increased risk of stroke, all-cause dementia, PD, and MS in IBD patients [ 42 ]. The GBA and gut microbiota dysbiosis are thought to play a role in the association between IBDs and neurodegenerative diseases [ 9 , 43 , 44 , 45 , 46 ].…”

Section: Is Neurodegeneration An Extraintestinal Manifestation Of Ibds?mentioning

confidence: 99%

“… Chronic inflammation is a hallmark of both IBDs and neurodegenerative diseases. Inflammatory mediators and immune cells can cross the BBB and contribute to neuroinflammation, neuronal damage, and neurodegeneration [ 43 , 47 , 48 , 49 ]. Increased oxidative stress, resulting from an imbalance between reactive oxygen species (ROS) production and antioxidant defense mechanisms, is implicated in the pathogenesis of both IBDs and neurodegenerative diseases [ 43 ].…”

Section: Is Neurodegeneration An Extraintestinal Manifestation Of Ibds?mentioning

confidence: 99%

“…Inflammatory mediators and immune cells can cross the BBB and contribute to neuroinflammation, neuronal damage, and neurodegeneration [ 43 , 47 , 48 , 49 ]. Increased oxidative stress, resulting from an imbalance between reactive oxygen species (ROS) production and antioxidant defense mechanisms, is implicated in the pathogenesis of both IBDs and neurodegenerative diseases [ 43 ]. The integrity of the BBB might be compromised in IBDs, allowing the entry of inflammatory mediators and immune cells into the CNS [ 43 ].…”

Section: Is Neurodegeneration An Extraintestinal Manifestation Of Ibds?mentioning

confidence: 99%

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From Gut to Brain: Uncovering Potential Serum Biomarkers Connecting Inflammatory Bowel Diseases to Neurodegenerative Diseases

Sarb,

Iacobescu

et al. 2024

IJMS

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Inflammatory bowel diseases (IBDs) are characterized by chronic gastrointestinal inflammation due to abnormal immune responses to gut microflora. The gut–brain axis is disrupted in IBDs, leading to neurobiological imbalances and affective symptoms. Systemic inflammation in IBDs affects the brain’s inflammatory response system, hormonal axis, and blood–brain barrier integrity, influencing the gut microbiota. This review aims to explore the association between dysregulations in the gut–brain axis, serum biomarkers, and the development of cognitive disorders. Studies suggest a potential association between IBDs and the development of neurodegeneration. The mechanisms include systemic inflammation, nutritional deficiency, GBA dysfunction, and the effect of genetics and comorbidities. The objective is to identify potential correlations and propose future research directions to understand the impact of altered microbiomes and intestinal barrier functions on neurodegeneration. Serum levels of vitamins, inflammatory and neuronal damage biomarkers, and neuronal growth factors have been investigated for their potential to predict the development of neurodegenerative diseases, but current results are inconclusive and require more studies.

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“…The gut-brain has a two-way regulatory function in nerve, endocrine, immunity, and metabolism, and is related to inflammatory bowel disease, obesity, diabetes, insulin resistance, and other gastrointestinal and metabolic diseases ( 6 ). Microorganisms that colonize the intestine play an indispensable role in brain and gut communication.…”

Section: Introductionmentioning

confidence: 99%

Intervention effects of low-molecular-weight chondroitin sulfate from the nasal cartilage of yellow cattle on lipopolysaccharide-induced behavioral disorders: regulation of the microbiome-gut-brain axis

Deng,

Li,

Song

et al. 2024

Front. Nutr.

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Chondroitin sulfate (CS) is a sulfated linear polysaccharide with different functional activities, including antioxidant, anti-inflammatory, lipid-lowering, and immune regulation. As natural sulfated polysaccharides have high molecular weight, high apparent viscosity, low water solubility, complex structure, and high negative charge, they have difficulty binding to receptors within cells across tissue barriers, resulting in low bioavailability and unclear structure–activity relationships. In this study, an H2O2-Vc oxidative degradation system was employed to perform environmentally friendly and controllable degradation of CS extracted from the nasal cartilage of Shaanxi Yellow cattle. Two low-molecular-weight chondroitin sulfates (LMWCSs), CS-1 (14.8 kDa) and CS-2 (50.9 kDa), that exhibit strong in vitro free radical scavenging ability were obtained, and their structures were characterized. Mice intraperitoneally administered lipopolysaccharide (LPS) were used to explore the cognitive intervention effects of LMWCS. Supplementing CS-1 and CS-2 significantly downregulated the levels of the serum inflammatory factors, TNF-α and IL-1β, promoted the expression of GSH in the brain, and inhibited the production of the lipid peroxidation product, malondialdehyde (MDA), ultimately inhibiting LPS-induced cognitive impairment in mice. Surprisingly, compared to the LPS model group, the abundances of Streptococcus, Eisenbergiella, Vampirovibrio, Coprococcus, Enterococcus and Lachnoanaerobaculum were significantly increased in the intestines of mice in the CS-1 and CS-2 group, whereas those of Parabacteroides and Mycoplasma were significantly decreased. Altogether, this study provides a theoretical basis for the comprehensive utilization of agricultural and animal resources and the application of brain nutrition, anti-inflammatory, and LMWCS health products.

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The Interface between Inflammatory Bowel Disease, Neuroinflammation, and Neurological Disorders

Cited by 4 publications

References 129 publications

Enteric Nervous System Alterations in Inflammatory Bowel Disease: Perspectives and Implications

Enteric Nervous System Alterations in Inflammatory Bowel Disease: Perspectives and Implications

From Gut to Brain: Uncovering Potential Serum Biomarkers Connecting Inflammatory Bowel Diseases to Neurodegenerative Diseases

Intervention effects of low-molecular-weight chondroitin sulfate from the nasal cartilage of yellow cattle on lipopolysaccharide-induced behavioral disorders: regulation of the microbiome-gut-brain axis

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