scholarly journals Intestinal epithelial glycosylation in homeostasis and gut microbiota interactions in IBD

2020 ◽  
Vol 17 (10) ◽  
pp. 597-617
Author(s):  
Matthew R. Kudelka ◽  
Sean R. Stowell ◽  
Richard D. Cummings ◽  
Andrew S. Neish
Keyword(s):  
Gut Microbiota ◽  
Intestinal Epithelial

scholarly journals IRF3 prevents colorectal tumorigenesis via inhibiting the nuclear translocation of β-catenin

2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Miao Tian ◽  
Xiumei Wang ◽  
Jihong Sun ◽  
Wenlong Lin ◽  
Lumin Chen ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Nuclear Translocation ◽  
Negative Regulator ◽  
Intestinal Epithelial ◽  
Colorectal Tumorigenesis ◽  
Genetic Ablation ◽  
Prognosis Marker ◽  
Immune Sensing ◽  
Innate Immune Sensing

AbstractOccurrence of Colorectal cancer (CRC) is relevant with gut microbiota. However, role of IRF3, a key signaling mediator in innate immune sensing, has been barely investigated in CRC. Here, we unexpectedly found that the IRF3 deficient mice are hyper-susceptible to the development of intestinal tumor in AOM/DSS and Apcmin/+ models. Genetic ablation of IRF3 profoundly promotes the proliferation of intestinal epithelial cells via aberrantly activating Wnt signaling. Mechanically, IRF3 in resting state robustly associates with the active β-catenin in the cytoplasm, thus preventing its nuclear translocation and cell proliferation, which can be relieved upon microbe-induced activation of IRF3. In accordance, the survival of CRC is clinically correlated with the expression level of IRF3. Therefore, our study identifies IRF3 as a negative regulator of the Wnt/β-catenin pathway and a potential prognosis marker for Wnt-related tumorigenesis, and describes an intriguing link between gut microbiota and CRC via the IRF3-β-catenin axis.

scholarly journals 376 – Interleukin-33 Promotes Reg3G Expression in Intestinal Epithelial Cells and Regulates Gut Microbiota

2019 ◽  
Vol 156 (6) ◽  
pp. S-78
Author(s):  
Wenjing Yang ◽  
Yi Xiao ◽  
Xiangsheng Huang ◽  
Suxia Yao ◽  
Zhanju Liu ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Gut Microbiota ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial ◽  
Interleukin 33

scholarly journals PTU-066 The gut microbiota influences intestinal epithelial proliferative potential

2018 ◽  
Author(s):  
John P Thomas ◽  
Aimee Parker ◽  
Devina Divekar ◽  
Carmen Pin ◽  
Alastair Watson
Keyword(s):  
Gut Microbiota ◽  
Proliferative Potential ◽  
Intestinal Epithelial

scholarly journals Advanced Organ-on-a-Chip Devices to Investigate Liver Multi-Organ Communication: Focus on Gut, Microbiota and Brain

2019 ◽  
Vol 6 (4) ◽  
pp. 91 ◽  
Author(s):  
Lucia Boeri ◽  
Luca Izzo ◽  
Lorenzo Sardelli ◽  
Marta Tunesi ◽  
Diego Albani ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Epithelial Barrier ◽  
Intestinal Epithelial ◽  
Barrier Dysfunction ◽  
In Vitro Modeling ◽  
Reciprocal Influence ◽  
Organ On A Chip ◽  
Epithelial Barrier Dysfunction

The liver is a key organ that can communicate with many other districts of the human body. In the last few decades, much interest has focused on the interaction between the liver and the gut microbiota, with their reciprocal influence on biosynthesis pathways and the integrity the intestinal epithelial barrier. Dysbiosis or liver disorders lead to0 epithelial barrier dysfunction, altering membrane permeability to toxins. Clinical and experimental evidence shows that the permeability hence the delivery of neurotoxins such as LPS, ammonia and salsolinol contribute to neurological disorders. These findings suggested multi-organ communication between the gut microbiota, the liver and the brain. With a view to in vitro modeling this liver-based multi-organ communication, we describe the latest advanced liver-on-a-chip devices and discuss the need for new organ-on-a-chip platforms for in vitro modeling the in vivo multi-organ connection pathways in physiological and pathological situations.

Flaxseed oligosaccharides alleviate DSS-induced colitis through modulation of gut microbiota and repair of the intestinal barrier in mice

2020 ◽  
Vol 11 (9) ◽  
pp. 8077-8088
Author(s):  
Zhenxia Xu ◽  
Wenchao Chen ◽  
Qianchun Deng ◽  
Qingde Huang ◽  
Xu Wang ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Intestinal Barrier ◽  
Epithelial Barrier ◽  
Intestinal Epithelial ◽  
Barrier Dysfunction ◽  
Intestinal Epithelial Barrier ◽  
Epithelial Barrier Dysfunction

Intestinal epithelial barrier dysfunction with dysbiosis of gut microbiota contributes to the occurrence and acceleration of colitis.

scholarly journals Organoid-based models to study the role of host-microbiota interactions in IBD

2020 ◽  
Author(s):  
Martina Poletti ◽  
Kaline Arnauts ◽  
Marc Ferrante ◽  
Tamas Korcsmaros
Keyword(s):  
Gut Microbiota ◽  
Ex Vivo ◽  
Disease Onset ◽  
Intestinal Epithelial ◽  
Cell Level ◽  
Disease Mechanisms ◽  
Microbial Screening ◽  
Inflammatory Bowel ◽  
Research Questions

Abstract The gut microbiota appears to play a central role in health, and alterations in the gut microbiota are observed in both forms of Inflammatory Bowel Disease (IBD), namely Crohn’s disease and ulcerative colitis. Yet, the mechanisms behind host-microbiota interactions in IBD, especially at the intestinal epithelial cell level, are not yet fully understood. Dissecting the role of host-microbiota interactions in disease onset and progression is pivotal, and requires representative models mimicking the gastrointestinal ecosystem, including the intestinal epithelium, the gut microbiota and immune cells. New advancements in organoid microfluidics technology are facilitating the study of IBD-related microbial-epithelial crosstalk, and the discovery of novel microbial therapies. Here, we review different organoid-based ex vivo models that are currently available, and benchmark their suitability and limitations for specific research questions. Organoid applications such as patient-derived organoid biobanks for microbial screening and omics technologies are discussed, highlighting their potential to gain better mechanistic insights into disease mechanisms and eventually allowing personalized medicine.

scholarly journals The phytonutrient cinnamaldehyde limits intestinal inflammation and enteric parasite infection

2021 ◽  
Author(s):  
Ling Zhu ◽  
Audrey I.S. Andersen-Civil ◽  
Laura J. Myhill ◽  
Stig M. Thamsborg ◽  
Witold Kot ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Metabolic Diseases ◽  
Intestinal Inflammation ◽  
Inflammatory Responses ◽  
Host Responses ◽  
Mucosal Inflammation ◽  
Enteric Infection ◽  
Intestinal Epithelial ◽  
Mesenteric Lymph Nodes

AbstractPhytonutrients such as cinnamaldehyde (CA) have been studied for their effects on metabolic diseases, but their influence on mucosal inflammation and immunity to enteric infection are not well documented. Here, we show that consumption of CA significantly down-regulates transcriptional pathways connected to inflammation in the small intestine of mice. During infection with the enteric helminth Heligomosomoides polygyrus, CA-treated mice displayed higher growth rates and less worms, concomitant with altered T-cell populations in mesenteric lymph nodes. Furthermore, infection-induced changes in gene pathways connected to cell cycle and mitotic activity were counteracted by CA. Mechanically, CA did not appear to exert activity through a prebiotic effect, as CA treatment did not significantly change the composition of the gut microbiota. Instead, in vitro experiments showed that CA directly induced xenobiotic metabolizing pathways in intestinal epithelial cells and suppressed endotoxin-induced inflammatory responses in macrophages. Thus, CA down-regulates inflammatory pathways in the intestinal mucosa and regulates host responses to enteric infection. These properties appear to be largely independent of the gut microbiota and instead connected to CA’s ability to induce antioxidant pathways in intestinal cells. Our results encourage further investigation into the use of CA and related phytonutrients as functional food components to promote intestinal health in humans and animals.

scholarly journals Inflammatory and Microbiota-Related Regulation of the Intestinal Epithelial Barrier

2021 ◽  
Vol 8 ◽  
Author(s):  
Giovanni Barbara ◽  
Maria Raffaella Barbaro ◽  
Daniele Fuschi ◽  
Marta Palombo ◽  
Francesca Falangone ◽  
...  
Keyword(s):  
Immune System ◽  
Gut Microbiota ◽  
Cell Damage ◽  
Short Chain Fatty Acids ◽  
The Body ◽  
Epithelial Barrier ◽  
Intestinal Epithelial ◽  
Intestinal Epithelial Barrier ◽  
Inflammatory Bowel ◽  
Irritable Bowel

The intestinal epithelial barrier (IEB) is one of the largest interfaces between the environment and the internal milieu of the body. It is essential to limit the passage of harmful antigens and microorganisms and, on the other side, to assure the absorption of nutrients and water. The maintenance of this delicate equilibrium is tightly regulated as it is essential for human homeostasis. Luminal solutes and ions can pass across the IEB via two main routes: the transcellular pathway or the paracellular pathway. Tight junctions (TJs) are a multi-protein complex responsible for the regulation of paracellular permeability. TJs control the passage of antigens through the IEB and have a key role in maintaining barrier integrity. Several factors, including cytokines, gut microbiota, and dietary components are known to regulate intestinal TJs. Gut microbiota participates in several human functions including the modulation of epithelial cells and immune system through the release of several metabolites, such as short-chain fatty acids (SCFAs). Mediators released by immune cells can induce epithelial cell damage and TJs dysfunction. The subsequent disruption of the IEB allows the passage of antigens into the mucosa leading to further inflammation. Growing evidence indicates that dysbiosis, immune activation, and IEB dysfunction have a role in several diseases, including irritable bowel syndrome (IBS), inflammatory bowel disease (IBD), and gluten-related conditions. Here we summarize the interplay between the IEB and gut microbiota and mucosal immune system and their involvement in IBS, IBD, and gluten-related disorders.

scholarly journals Phillygenin Attenuates Carbon Tetrachloride-Induced Liver Fibrosis via Modulating Inflammation and Gut Microbiota

2021 ◽  
Vol 12 ◽  
Author(s):  
Cheng Wang ◽  
Cheng Ma ◽  
Ke Fu ◽  
Li-Hong Gong ◽  
Ya-Fang Zhang ◽  
...  
Keyword(s):  
Carbon Tetrachloride ◽  
Liver Fibrosis ◽  
Liver Function ◽  
Gut Microbiota ◽  
Epithelial Barrier ◽  
Rrna Gene ◽  
Intestinal Epithelial ◽  
Collagen Deposition ◽  
Intestinal Epithelial Barrier ◽  
Corrective Effect

Liver fibrosis is a chronic pathological process that various pathogenic factors lead to abnormal hyperplasia of hepatic connective tissue, and its main feature is the excessive deposition of extracellular matrix. However, there are currently no drugs approved for the treatment of liver fibrosis. Phillygenin (PHI), a lignan isolated from Forsythiae Fructus, showed potential anti-inflammatory and anti-fibrosis effects but the mechanisms remain unknown. In view of the vital role of gut microbiota in the development of liver fibrosis, this study aimed to explore whether PHI could protect intestinal epithelial barrier and attenuate liver fibrosis by maintaining the homeostasis of intestinal microbiota. Therefore, the liver fibrosis model was induced by intraperitoneal injection of olive oil containing 10% carbon tetrachloride (CCl4) for 4 weeks in C57BL/6J mice. Histological analysis including Hematoxylin-Eosin, Masson, Sirius red, and immunohistochemistry staining were carried out to detect the histopathology and collagen deposition of mice liver tissues. The biochemical indexes related to liver function (ALT, AST, AKP, γ-GT), fibrosis (HYP, HAase, LN, PC III, IV-C) and inflammation (TNF-α, MIP-1, LPS) were determined by specific commercial assay kits. In vivo experimental results showed that PHI could improve liver histopathological injury, abnormal liver function, collagen deposition, inflammation and fibrosis caused by CCl4. Moreover, PHI restored the intestinal epithelial barrier by promoting the expression of intestinal barrier markers, including ZO-1, Occludin and Claudin-1. More importantly, the corrective effect of PHI on the imbalance of gut microbiota was confirmed by sequencing of the 16 S rRNA gene. In particular, PHI treatment enriches the relative abundance of Lactobacillus, which is reported to alleviate inflammation and fibrosis of damaged liver. Collectively, PHI attenuates CCl4-induced liver fibrosis partly via modulating inflammation and gut microbiota.

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