scholarly journals Erratum: Corrigendum: EpCAM-dependent extracellular vesicles from intestinal epithelial cells maintain intestinal tract immune balance

2017 ◽  
Vol 8 (1) ◽  
Author(s):  
Lingling Jiang ◽  
Yingying Shen ◽  
Danfeng Guo ◽  
Diya Yang ◽  
Jiajun Liu ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Extracellular Vesicles ◽  
Intestinal Tract ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial ◽  
Immune Balance

scholarly journals EpCAM-dependent extracellular vesicles from intestinal epithelial cells maintain intestinal tract immune balance

2016 ◽  
Vol 7 (1) ◽  
Author(s):  
Lingling Jiang ◽  
Yingying Shen ◽  
Danfeng Guo ◽  
Diya Yang ◽  
Jiajun Liu ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Extracellular Vesicles ◽  
Intestinal Tract ◽  
Intestinal Epithelial Cells ◽  
Dependent Manner ◽  
Intestinal Epithelial ◽  
Immune Balance ◽  
Inflammatory Bowel ◽  
Tgf Β1

Abstract How the intestinal tract develops a tolerance to foreign antigens is still largely unknown. Here we report that extracellular vesicles (EVs) with TGF-β1-dependent immunosuppressive activity are produced by intestinal epithelial cells (IECs) under physiological conditions. Transfer of these EVs into inflammatory bowel disease (IBD) mice induced by dextran sulfate sodium salt decreases IBD severity by inducing regulatory T cells and immunosuppressive dendritic cells. In contrast, decreased endogenous EV production promotes IBD development. IECs produce EVs with increased levels of TGF-β1 upon IBD development in an ERK-dependent manner. Furthermore, these EVs tend to localize in the intestinal tract associated with epithelial cell adhesion molecule (EpCAM). Knockdown of EpCAM in vivo increases the severity of murine IBD, and the protective effect of EVs from IECs with decreased EpCAM on murine IBD is blunted. Therefore, our study indicates that EVs from IECs participate in maintaining the intestinal tract immune balance.

scholarly journals Differential expression of endothelin-2 along the mouse intestinal tract

2005 ◽  
Vol 35 (2) ◽  
pp. 201-209 ◽  
Author(s):  
Satoshi Takizawa ◽  
Tsuyoshi Uchide ◽  
Javier Adur ◽  
Takaharu Kozakai ◽  
Eiichi Kotake-Nara ◽  
...  
Keyword(s):  
Gastrointestinal Tract ◽  
Epithelial Cells ◽  
Intestinal Tract ◽  
Intestinal Epithelial Cells ◽  
Immunohistochemical Analysis ◽  
Pcr Analysis ◽  
Intestinal Epithelial ◽  
Peyer’S Patch ◽  
Peyer's Patch ◽  
Specific Distribution

Endothelin (ET)-2, an ET family peptide, is highly expressed in intestine. However, the specific distribution and function of ET-2 remain unknown. We elucidated the expression profile and localization of ET-2 in mouse gastrointestinal tract. Real-time PCR analysis revealed that ET-2 gene expression in the gastrointestinal tract of healthy animals was relatively high in the colon. Immunohistochemical analysis revealed ET-2-like immunoreactivity mainly in epithelial cells of the mucosa throughout the intestinal tract of healthy animals. Intracellularly, ET-2 was concentrated close to the basement membrane of intestinal epithelial cells. A weak ET-2-like immunoreactivity was also localized to some neurofibers and the myenteric plexus of the muscle layer, coexpressing with vasoactive intestinal peptide. ET-2-like immunoreactivity was also detected at Brunner’s glands of the duodenum and follicle-associated epithelium of Peyer’s patch. In contrast, ET-1-like immunoreactivity was uniformly distributed in epithelial cells. In dextran sulfate sodium (DSS)-induced colitis, colonic ET-2 was upregulated during the late stage of DSS treatment. These results suggest that in intestinal epithelial cells ET-2 could be secreted into the lamina propria and the dome region in Peyer’s patch, and that it might modulate immune cells in these sites for mucosal defense.

Extracellular Vesicles: A New Nano Tool for the Treatment of Inflammatory Bowel Diseases

2019 ◽  
Vol 15 (6) ◽  
pp. 589-595
Author(s):  
Nitin Tandra ◽  
Peipei Wu ◽  
Xinyuan Hu ◽  
Fei Mao ◽  
Wenrong Xu ◽  
...  
Keyword(s):  
Extracellular Vesicles ◽  
Intestinal Tract ◽  
Intestinal Epithelial Cells ◽  
Therapeutic Strategies ◽  
Intestinal Stem Cells ◽  
Inflammatory Disorder ◽  
Intestinal Epithelial ◽  
Bowel Diseases ◽  
Inflammatory Bowel

The intestinal tract is a complex and important physiological and immunological organ. Intestinal tract homeostasis requires a series of coordinated interactions involving gut microbiota, the crypt intestinal stem cells (ISC) and the surrounding niche, including the intestinal epithelial cells, endothelial cells, dendritic cells, and macrophages. The destruction of intestinal homeostasis leads to autoimmune diseases, such as inflammatory bowel disease (IBD). IBD is a non-specific, and remittent- relapsing inflammatory disorder of the gastrointestinal tract. There is no effective method to keep patients in remission for a long term. It has been reported that extracellular vesicles (EVs) exert immune activation and immunosuppressive effects in the pathogenesis of IBD. In order to explore new therapeutic strategies for IBD, in this review, we summarize the observations on the immune properties and functions of EVs in intestinal mucosal immunity.

scholarly journals Specific and Non-Invasive Fluorescent Labelling of Extracellular Vesicles for Evaluation of Intracellular Processing by Intestinal Epithelial Cells

Biomedicines ◽  
2020 ◽  
Vol 8 (7) ◽  
pp. 211
Author(s):  
Maria S. Hansen ◽  
Ida S. E. Gadegaard ◽  
Eva C. Arnspang ◽  
Kristine Blans ◽  
Lene N. Nejsum ◽  
...  
Keyword(s):  
Immune System ◽  
Epithelial Cells ◽  
Fluorescence Microscopy ◽  
Cell Line ◽  
Extracellular Vesicles ◽  
Intestinal Epithelial Cells ◽  
Time Dependent ◽  
Intestinal Epithelial ◽  
Fluorescent Labelling ◽  
Non Invasive

The presence of extracellular vesicles (EVs) in milk has gained interest due to their capacity to modulate the infant’s intestinal and immune system. Studies suggest that milk EVs are enriched in immune-modulating proteins and miRNA, highlighting their possible health benefits to infants. To assess uptake of milk EVs by intestinal epithelial cells, a method was developed using labelling of isolated EVs with fluorophore-conjugated lactadherin. Lactadherin is a generic and validated EV marker, which enables an effective labelling of phosphatidylserine (PS) exposing EVs. Labelled EVs could effectively be used to describe a dose- and time-dependent uptake into the intestinal epithelial Caco-2 cell line. Additionally, fluorescence microscopy was employed to show that EVs colocalize with endosomal markers and lysosomes, indicating that EVs are taken up via general endocytotic mechanisms. Collectively, a method to specifically label isolated EVs is presented and employed to study the uptake of milk EVs by intestinal epithelial cells.

scholarly journals Production of a Functional Factor, p40, by Lactobacillus rhamnosus GG Is Promoted by Intestinal Epithelial Cell-Secreted Extracellular Vesicles

2019 ◽  
Vol 87 (7) ◽  
Author(s):  
Luyao Yang ◽  
James N. Higginbotham ◽  
Liping Liu ◽  
Gang Zhao ◽  
Sari A. Acra ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Epithelial Cells ◽  
Extracellular Vesicles ◽  
Gut Microbiome ◽  
Intestinal Inflammation ◽  
Intestinal Epithelial Cells ◽  
Lactobacillus Rhamnosus ◽  
Intestinal Epithelial ◽  
Colonic Epithelial Cell ◽  
Gut Microbes

ABSTRACT The symbiotic relationship between the gut microbiome and the host provides a nutrient-rich environment for gut microbes and has beneficial effects on host health. Although the composition of the gut microbiome is known to be influenced by both host genetics and environmental factors, host effects on the activities and functions of the gut microbial communities remain poorly understood. Intestinal epithelial cells exert front-line responses to gut microbes and contribute to maintaining a healthy intestinal homeostasis. Here, seeking to elucidate whether intestinal epithelial cells modulate Lactobacillus rhamnosus GG (LGG) functions, we examined the production of p40, an LGG-derived secretory protein that protects intestinal epithelial cells against inflammation. We found that growth medium conditioned with colonic epithelial cell-derived components promotes p40 protein synthesis and secretion by LGG and enhances LGG-stimulated protective responses in intestinal epithelial cells. Furthermore, when LGG was cultured with the colonic luminal contents from healthy mice, p40 production was upregulated but was attenuated with luminal contents from mice with intestinal inflammation. Importantly, the colonic epithelial cell-derived components potentiated LGG-produced p40 levels in a mouse model of colitis and enhanced LGG-mediated amelioration of intestinal inflammation in this model. Notably, we found that colonic epithelial cell-secreted extracellular vesicles participate in communicating with LGG and that heat shock protein 90 (HSP90) in these vesicles might mediate the promotion of p40 production. These results reveal a previously unrecognized mechanism by which the anti-inflammatory effect of LGG is reinforced by intestinal epithelial cells and thereby maintains intestinal health.

scholarly journals Intestinal Epithelial Cell-Derived Extracellular Vesicles Modulate Hepatic Injury via the Gut-Liver Axis During Acute Alcohol Injury

2020 ◽  
Vol 11 ◽  
Author(s):  
Arantza Lamas-Paz ◽  
Laura Morán ◽  
Jin Peng ◽  
Beatriz Salinas ◽  
Nuria López-Alcántara ◽  
...  
Keyword(s):  
Single Dose ◽  
Epithelial Cells ◽  
Binge Drinking ◽  
Extracellular Vesicles ◽  
Lipid Accumulation ◽  
Hepatic Injury ◽  
Intestinal Epithelial Cells ◽  
Heavy Episodic Drinking ◽  
Intestinal Epithelial ◽  
Alcohol Injury

Binge drinking, i.e., heavy episodic drinking in a short time, has recently become an alarming societal problem with negative health impact. However, the harmful effects of acute alcohol injury in the gut-liver axis remain elusive. Hence, we focused on the physiological and pathological changes and the underlying mechanisms of experimental binge drinking in the context of the gut-liver axis. Eight-week-old mice with a C57BL/6 background received a single dose (p.o.) of ethanol (EtOH) [6 g/kg b.w.] as a preclinical model of acute alcohol injury. Controls received a single dose of PBS. Mice were sacrificed 8 h later. In parallel, HepaRGs and Caco-2 cells, human cell lines of differentiated hepatocytes and intestinal epithelial cells intestinal epithelial cells (IECs), respectively, were challenged in the presence or absence of EtOH [0–100 mM]. Extracellular vesicles (EVs) isolated by ultracentrifugation from culture media of IECs were added to hepatocyte cell cultures. Increased intestinal permeability, loss of zonula occludens-1 (ZO-1) and MUCIN-2 expression, and alterations in microbiota—increased Lactobacillus and decreased Lachnospiraceae species—were found in the large intestine of mice exposed to EtOH. Increased TUNEL-positive cells, infiltration of CD11b-positive immune cells, pro-inflammatory cytokines (e.g., tlr4, tnf, il1β), and markers of lipid accumulation (Oil Red O, srbep1) were evident in livers of mice exposed to EtOH, particularly in females. In vitro experiments indicated that EVs released by IECs in response to ethanol exerted a deleterious effect on hepatocyte viability and lipid accumulation. Overall, our data identified a novel mechanism responsible for driving hepatic injury in the gut-liver axis, opening novel avenues for therapy.

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