Discoidin domain receptor 1(DDR1) promote intestinal barrier disruption in Ulcerative Colitis through tight junction proteins degradation and epithelium apoptosis

Li, Xiaoli; Li, Qianqian; Xiong, Bin; Chen, Huiling; Wang, Xiaochun; Zhang, Dekui

doi:10.1016/j.phrs.2022.106368

Cited by 26 publications

(12 citation statements)

References 39 publications

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“…We next ranked them based on the correlation of their expression within CC5 spots (see Methods, top 20 shown in Fig 3a ). Several of the significantly co-occurring LR pairs were previously implicated in colitis, and are mostly involved in epithelial integrity and repair ( DDR1-CDH1 15 , DSG2 16 ), immune recruitment ( MIF-CD74 17 ), and TNF signaling ( GRN-TNFRSF1A 18,19 ). This highlights ISCHIA’s ability to capture disease-relevant pathways from spatial transcriptomics data, even at a limited sample size.…”

Section: Resultsmentioning

confidence: 99%

Identifying Spatial Co-occurrence in Healthy and InflAmed tissues (ISCHIA)

Lafzi

Borrelli

Bach

et al. 2023

Preprint

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Spatial transcriptomics (ST) techniques are able to chart the distribution and localization of cell types and RNA molecules across a tissue. Sequencing-based methods allow unbiased capturing of RNA molecules at barcoded spots. While the coarse resolution of these techniquee is considered a disadvantage, we argue that the inherent proximity of transcriptomes captured on spots can be leveraged to reconstruct cellular networks. To this end, we developed ISCHIA (Identifying Spatial Co-occurrence in Healthy and InflAmed tissues), a computational framework to analyze the spatial co-occurrence of cell types and transcript species in the tissue environment. Co-occurrence analysis is complementary to differential gene expression, as it does not depend on the abundance of a given cell type or the transcript expression levels, but rather on their spatial arrangement in the tissue. We applied ISCHIA to analyze co-occurrence of cell types, ligands and receptors in a sequencing-based ST dataset of human ulcerative colitis, and validated our findings on matched hybridization-based data. We uncover inflammation-induced cellular networks involving M-cell and fibroblasts, as well as ligand-receptor interactions enriched in the inflamed human colon, and their associated gene signatures. Our results highlight the hypothesis-generating power and broad applicability of co-occurrence analysis on spatial transcriptomics data.

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Section: Resultsmentioning

confidence: 99%

Identifying Spatial Co-occurrence in Healthy and InflAmed tissues (ISCHIA)

Lafzi

Borrelli

Bach

et al. 2023

Preprint

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“…37 Losing TJ proteins is a crucial factor leading to barrier destruction in DSS-induced colitis. 38 Wheat germ active peptide APE can promote the expression of intestinal TJ proteins in colitis mice. Although UC patients can be treated with steroids, immunomodulators, antibodies, and other drugs, their use is limited by a series of side effects.…”

Section: ■ Discussionmentioning

confidence: 99%

“…The intestinal epithelial barrier is destroyed, and the permeability is increased, which can easily cause intestinal mucosal inflammation . Losing TJ proteins is a crucial factor leading to barrier destruction in DSS-induced colitis . Wheat germ active peptide APE can promote the expression of intestinal TJ proteins in colitis mice.…”

Section: Discussionmentioning

confidence: 99%

Wheat Germ-Derived Peptide Alleviates Dextran Sulfate Sodium-Induced Colitis in Mice

Wang,

Chen,

Itagaki

et al. 2023

J. Agric. Food Chem.

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This study explores the protective properties and potential mechanisms of wheat-germ-derived peptide APEPEPAF (APE) against ulcerative colitis. Colitis mice induced by dextran sulfate sodium (DSS) were used as the animal model. The results showed that the APE peptide could alleviate colitis symptoms including weight loss, colon shortening, and histopathological changes. This peptide attenuated the generation of inflammatory cytokines by inhibiting the phosphorylation of protein kinase PKCζ (Thr410) and NF-κB transcriptional activity in DSS-induced mice, suggesting that APE ameliorates colitis inflammation by regulating the PKCζ/NF-κB signaling pathway. APE also preserved the barrier function of the colon by dose-dependently promoting the expression of tight junction proteins (claudin-1, zonula occluded-1, and occludin). In addition, APE significantly decreased the abundance of Bacteroides and increased the abundance of Dubosiella and Lachnospiraceae_UCG-006 to improve the intestinal flora imbalance in DSS-induced colitis mice. Therefore, wheat germ peptide APE can be used as a novel agent and dietary supplement to treat ulcerative colitis..

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“…Hiengrach et al found that oral Candida can promote the growth of intestinal bacteria thereby inducing intestinal ecological dysbiosis, which in turn promotes colonic inflammation (Hiengrach et al, 2020); Candida albicans colonize the gut significantly more frequently and with greater severity in patients with CD than in the healthy population (Standaert-Vitse et al, 2009), whereas reducing intestinal fungus reduces the severity of the disease. Furthermore, in the study by Li et al oral Candida can colonize the gut through the digestive tract and disrupt the intestinal barrier by inducing the release of proinflammatory factors, while in the pathogenic mechanism of Candida candidalysin is a key virulence factor in promoting the inflammatory response in the gut (Li et al, 2022b). Oral Candida colonizes the intestine through the digestive tract and thus affects the metabolic and ecological balance of the flora.…”

Section: Microbial Associations Of Periodontitis and Ibdmentioning

confidence: 99%

The effect of the “Oral-Gut” axis on periodontitis in inflammatory bowel disease: A review of microbe and immune mechanism associations

Zhou

Wang

et al. 2023

Front. Cell. Infect. Microbiol.

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Periodontitis and inflammatory bowel diseases (IBD) are inflammatory diseases of the gastrointestinal tract that share common features of microbial-induced ecological dysregulation and host immune inflammatory response. The close relationship between periodontitis and IBD is characterized by a higher prevalence of IBD in patients with periodontitis and a higher prevalence and severity of periodontitis in patients with IBD, indicating that periodontitis and IBD are different from the traditional independent diseases and form an “Oral-Gut” axis between the two, which affect each other and thus form a vicious circle. However, the specific mechanisms leading to the association between the two are not fully understood. In this article, we describe the interconnection between periodontitis and IBD in terms of microbial pathogenesis and immune dysregulation, including the ectopic colonization of the gut by pathogenic bacteria associated with periodontitis that promotes inflammation in the gut by activating the host immune response, and the alteration of the oral microbiota due to IBD that affects the periodontal inflammatory response. Among the microbial factors, pathogenic bacteria such as Klebsiella, Porphyromonas gingivalis and Fusobacterium nucleatum may act as the microbial bridge between periodontitis and IBD, while among the immune mechanisms, Th17 cell responses and the secreted pro-inflammatory factors IL-1β, IL-6 and TNF-α play a key role in the development of both diseases. This suggests that in future studies, we can look for targets in the “Oral-Gut” axis to control and intervene in periodontal inflammation by regulating periodontal or intestinal flora through immunological methods.

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Discoidin domain receptor 1(DDR1) promote intestinal barrier disruption in Ulcerative Colitis through tight junction proteins degradation and epithelium apoptosis

Cited by 26 publications

References 39 publications

Identifying Spatial Co-occurrence in Healthy and InflAmed tissues (ISCHIA)

Identifying Spatial Co-occurrence in Healthy and InflAmed tissues (ISCHIA)

Wheat Germ-Derived Peptide Alleviates Dextran Sulfate Sodium-Induced Colitis in Mice

The effect of the “Oral-Gut” axis on periodontitis in inflammatory bowel disease: A review of microbe and immune mechanism associations

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