Slimy partners: the mucus barrier and gut microbiome in ulcerative colitis

Fang, Jian; Wang, Hui; Zhou, Yuping; Zhang, Hui; Zhou, Huiting; Zhang, Xiaohong

doi:10.1038/s12276-021-00617-8

Cited by 128 publications

(92 citation statements)

References 142 publications

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“…Considering one of the hallmarks of PPE lesions is the loss of goblet cells and the protective intestinal mucin layer (1,37), it is likely that bacteria other than L. intracellularis could contribute to the development of lesions as they would have increased access to the epithelium. Additionally, mucin is known to harbor antimicrobial peptides, which, if altered during infection, could also contribute to dysbiosis (38,39).…”

Section: Discussionmentioning

confidence: 99%

Oral Vaccination Reduces the Effects of Lawsonia intracellularis Challenge on the Swine Small and Large Intestine Microbiome

et al. 2021

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Porcine proliferative enteropathy remains one of the most prevalent diseases in swine herds worldwide. This disease is caused by Lawsonia intracellularis, an intracellular bacterial pathogen that primarily colonizes the ileum. In this study, we evaluated changes to the microbiome of the ileal mucosa, ileal digesta, cecal digesta, and feces subsequent to challenge with L. intracellularis and to an oral live vaccine against L. intracellularis. Given that gut homogenates have been used since 1931 to study this disease, we also characterized the microbial composition of a gut homogenate from swine infected with L. intracellularis that was used as challenge material. The L. intracellularis challenge led to a dysbiosis of the microbiome of both the small and large intestine marked by an increase of pathobionts including Collinsella, Campylobacter, Chlamydia, and Fusobacterium. This microbiome response could play a role in favoring L. intracellularis colonization and disease as well as potentially predisposing to other diseases. Vaccination altered both small and large intestine microbiome community structure and led to a significant 3.03 log10 reduction in the amount of L. intracellularis shed by the challenged pigs. Vaccination also led to a significant decrease in the abundance of Collinsella, Fusobacterium, and Campylobacter among other microbial changes compared with non-vaccinated and challenged animals. These results indicate that L. intracellularis infection is associated with broad changes to microbiome composition in both the large and small intestine, many of which can be mitigated by vaccination.

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Section: Discussionmentioning

confidence: 99%

Oral Vaccination Reduces the Effects of Lawsonia intracellularis Challenge on the Swine Small and Large Intestine Microbiome

et al. 2021

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“…β-defensin expression is known to be regulated by MUC2, a major component of the mucus layer in the gut which serves as an additional barrier between gut microbes and epithelial cells [29]. The mucus layer is also composed of a loose outer layer colonized by the gut microbiota and a firmer inner layer which serves as a diffusion barrier, separating the microbiota from epithelial cells [80]. The study by Gao et al [29] showed that 4 weeks of CRS was sufficient to decrease colonic MUC2 expression and goblet cell numbers.…”

Section: Intestinal Barrier Integrity Pathwaysmentioning

confidence: 99%

The Effects of Stress and Diet on the “Brain–Gut” and “Gut–Brain” Pathways in Animal Models of Stress and Depression

Herselman

Bailey

Bobrovskaya

2022

IJMS

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Compelling evidence is building for the involvement of the complex, bidirectional communication axis between the gastrointestinal tract and the brain in neuropsychiatric disorders such as depression. With depression projected to be the number one health concern by 2030 and its pathophysiology yet to be fully elucidated, a comprehensive understanding of the interactions between environmental factors, such as stress and diet, with the neurobiology of depression is needed. In this review, the latest research on the effects of stress on the bidirectional connections between the brain and the gut across the most widely used animal models of stress and depression is summarised, followed by comparisons of the diversity and composition of the gut microbiota across animal models of stress and depression with possible implications for the gut–brain axis and the impact of dietary changes on these. The composition of the gut microbiota was consistently altered across the animal models investigated, although differences between each of the studies and models existed. Chronic stressors appeared to have negative effects on both brain and gut health, while supplementation with prebiotics and/or probiotics show promise in alleviating depression pathophysiology.

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“…We found that Axin1 ΔIEC mice are protected from DSS-induced inflammation but have a weakened mucus barrier. It’s been shown that a depleted mucus barrier results in susceptibility to DSS-induced colitis [48, 49, 50]. However, increased Muc2 and Akkermansia muciniphilia have been shown to protect against DSS-colitis [30, 50], which collectively may allow the Axin1 ΔIEC mice to have increased colitis-protection compared to controls.…”

Section: Discussionmentioning

confidence: 99%

Intestinal epithelial Axin1 deficiency protects against colitis via altered gut microbiota

Garrett

Zhang

Xia

et al. 2022

Preprint

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Background and Aims: Intestinal homeostasis is maintained by specialized host cells and the gut microbiota. Wnt/β-catenin signaling is essential for gastrointestinal development and homeostasis, and its dysregulation has been implicated in inflammation and colorectal cancer. Axin1 negatively regulates activated Wnt/β-catenin signaling, but little is known regarding its role in regulating host-microbial interactions in health and disease. Here, we aim to demonstrate that intestinal Axin1 determines gut homeostasis and host response to inflammation. Methods: The expression of Axin1 was analyzed in human IBD datasets. To explore the effects and mechanism of intestinal Axin1 in regulating intestinal homeostasis and colitis, we generated mouse models with Axin1 conditional knockout in intestinal epithelial (Axin1∆IEC) and Paneth cells (Axin1∆PC) to compare with control (Axin1LoxP) mice. Results: We found increased Axin1 expression in the colonic epithelium of human IBD. Axin1∆IEC mice exhibited altered goblet cell spatial distribution, Paneth cell morphology, reduced lysozyme expression, and enriched Akkermansia muciniphila. Absence of intestinal epithelial and Paneth cell Axin1 decreased susceptibility to DSS-induced colitis in vivo. Axin1∆IEC and Axin1∆PC became more susceptible to DSS-colitis after cohousing with control mice, suggesting the non-colitogenic effect is driven by the gut microbiota. Conclusion: We found loss of intestinal Axin1 protects against colitis, which is likely driven through Paneth cell Axin1 and the microbiota. Our study demonstrates a novel role of Axin1 in mediating intestinal homeostasis and the microbiota. Further mechanistic studies using specific Axin1 mutations elucidating how Axin1 modulates microbiome and host inflammatory response, will provide new therapeutic strategies for human IBD.

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Slimy partners: the mucus barrier and gut microbiome in ulcerative colitis

Cited by 128 publications

References 142 publications

Oral Vaccination Reduces the Effects of Lawsonia intracellularis Challenge on the Swine Small and Large Intestine Microbiome

Oral Vaccination Reduces the Effects of Lawsonia intracellularis Challenge on the Swine Small and Large Intestine Microbiome

The Effects of Stress and Diet on the “Brain–Gut” and “Gut–Brain” Pathways in Animal Models of Stress and Depression

Intestinal epithelial Axin1 deficiency protects against colitis via altered gut microbiota

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