Faecal microRNAs: indicators of imbalance at the host-microbe interface?

2018 ◽  
Vol 9 (2) ◽  
pp. 175-183 ◽  
Author(s):  
G.M. Moloney ◽  
M.F. Viola ◽  
A.E. Hoban ◽  
T.G. Dinan ◽  
J.F. Cryan
Keyword(s):  
Epithelial Cells ◽  
Gut Microbiota ◽  
Antibiotic Treatment ◽  
Mirna Expression ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial ◽  
Sprague Dawley ◽  
Faecal Pellets ◽  
Non Invasive ◽  
Bodily Fluids

The enteric microbiota is characterised by a balance and composition that is unique to the host. It is important to understand the mechanisms through which the host can maintain the composition of the gut microbiota. MicroRNAs (miRNA) are implicated in intercellular communication and have been isolated from bodily fluids including stool. Recent findings suggest that miRNA produced by the host’s intestinal epithelial cells (IECs) participate in shaping the microbiota. To investigate whether miRNA expression was influenced by the gut microbiota we measured the expression of miRNAs expressed by intestinal epithelial cells in faeces. Specifically, we measured miRNA expression in faeces from germ-free (GF) and conventional mice and similarly in a rat model of antibiotic-mediated depletion of the gut microbiota control rats. In adult male GF and conventional mice and adult Sprague Dawley (SD) rats were treated with a combination of antibiotics for 8 weeks; total RNA was extracted from faecal pellets taken at week 0, 2, 4, 6 week 8 and the expression of let-7b-3p, miR-141-3p, miR-200a-3p and miR-1224-5p (miRNAs known to be expressed in IECs) were measured relative to U6 at each time point using qRT-PCR. In GF animals the expression of let-7b, miR-141 and miR-200a in faeces was lower compared to conventional mice. Following antibiotic-mediated depletion of gut microbiota, rats showed two divergent profiles of miRNA expression. Following two weeks of antibiotic treatment, the expression of let-7b and miR-1224 dropped significantly and remained low for the remainder of the study. The expression of miR-200a and miR-141 was significantly higher at week 2 than before antibiotic treatment commenced. Subsequently, the expression of miR-200a and miR-141 decreased at week 4 and continued to decrease at week 6. This data demonstrates that miRNAs can be used as an independent, non-invasive marker of microbial fluctuations along with gut pathology in the intestine.

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 Identification and characteristics of postnatal development-related long non-coding RNAs under microbiota dependent condition

2020 ◽  
Author(s):  
Miaomiao Zheng ◽  
Binbin Zhang ◽  
Yidan Zhang ◽  
Tingting Sun ◽  
Baozhong Hu
Keyword(s):  
Epithelial Cells ◽  
Gut Microbiota ◽  
Postnatal Development ◽  
Intestinal Epithelial Cells ◽  
Development Stage ◽  
Intestinal Epithelial ◽  
Early Postnatal Development ◽  
Development Stages ◽  
Large Numbers ◽  
Non Coding Rnas

Abstract BackgroundThe interplay of long-non coding RNAs (lncRNAs) and the intestinal microbiota may serve as an essential role in intestinal development and homeostasis. Microbiota could regulate a large numbers of lncRNAs expression in intestinal epithelial cells. However, the associations between lncRNAs and microbiota during early postnatal development stages are still need to understand. MethodsIn present study, the microbial effects on lncRNA of intestinal epithelial cells (IECs) during postnatal development stage were investigated. ResultsWe identified gut microbiota-specific lncRNAs in diverse postnatal development stages including week 1, week 4 and week 12/16 of mice. A large proportion of gut microbiota-specific lncRNAs only were differential expressed in a single postnatal development stage. Up- and down-regulated gut microbiota-specific lncRNAs both showed consistent expression pattern. We also constructed gut microbiota-specific lncRNAs and coding genes interacted co-expressed networks. Functional analysis indicated that gut microbiota-specific lncRNAs were associated with ABC transporters. ConclusionsIn summary, the present study characterizes the landscape of lncRNAs associated with gut microbiota in different postnatal development stages. It provide assistance for exploring the relationships among lncRNAs, gut microbiota and postnatal development stages.

scholarly journals Hypoxic Environment Promotes Barrier Formation in Human Intestinal Epithelial Cells through Regulation of MicroRNA 320a Expression

2019 ◽  
Vol 39 (14) ◽  
Author(s):  
Stephanie Muenchau ◽  
Rosalie Deutsch ◽  
Ines J. de Castro ◽  
Thomas Hielscher ◽  
Nora Heber ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Mirna Expression ◽  
Barrier Function ◽  
Intestinal Epithelial Cells ◽  
Hypoxia Inducible Factor ◽  
Intestinal Epithelial ◽  
Low Oxygen ◽  
Direct Role ◽  
Hypoxic Conditions ◽  
Barrier Formation

ABSTRACT Intestinal epithelial cells (IECs) are exposed to the low-oxygen environment present in the lumen of the gut. These hypoxic conditions on one hand are fundamental for the survival of the commensal microbiota and, on the other hand, favor the formation of a selective semipermeable barrier, allowing IECs to transport essential nutrients/water while keeping the sterile internal compartments separated from the lumen containing commensals. The hypoxia-inducible factor (HIF) complex, which allows cells to respond and adapt to fluctuations in oxygen levels, has been described as a key regulator in maintaining IEC barrier function by regulating their tight junction integrity. In this study, we sought to better evaluate the mechanisms by which low oxygen conditions impact the barrier function of human IECs. By profiling miRNA expression in IECs under hypoxia, we identified microRNA 320a (miRNA-320a) as a novel barrier formation regulator. Using pharmacological inhibitors and short hairpin RNA-mediated silencing, we could demonstrate that expression of this microRNA (miRNA) was HIF dependent. Importantly, using overexpression and knockdown approaches of miRNA-320a, we could confirm its direct role in the regulation of barrier function in human IECs. These results reveal an important link between miRNA expression and barrier integrity, providing a novel insight into mechanisms of hypoxia-driven epithelial homeostasis.

scholarly journals Intestinal epithelial CD98 synthesis specifically modulates expression of colonic microRNAs during colitis

2012 ◽  
Vol 302 (11) ◽  
pp. G1282-G1291 ◽  
Author(s):  
Moiz A. Charania ◽  
Saravanan Ayyadurai ◽  
Sarah A. Ingersoll ◽  
Bo Xiao ◽  
Emilie Viennois ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Epithelial Cells ◽  
Mirna Expression ◽  
Target Genes ◽  
Immune Cell ◽  
Intestinal Inflammation ◽  
Intestinal Epithelial Cells ◽  
Cell Types ◽  
Intestinal Epithelial ◽  
Small Noncoding Rnas

The transmembrane glycoprotein CD98 is known to be involved in intestinal inflammation. In the present study, we found that CD98 overexpression in intestinal epithelial cells does not normally affect the expression of colonic (epithelial and immune cell) microRNAs (miRNAs), small noncoding RNAs that posttranscriptionally regulate a wide variety of biological processes. However, upon dextran sulfate sodium (DSS) treatment, the expression of several colonic miRNAs, but not miRNAs from other tissues such as liver and spleen, were differentially regulated in mice overexpressing CD98 in epithelial cells compared with wild-type (WT) animals. For example, the level of colonic miRNA 132 was not affected by DSS treatment in WT animals but was upregulated in mice overexpressing CD98 in intestinal epithelial cells. Other colonic miRNAs, including colonic miRNA 23a and 23b, were downregulated in WT animals after DSS treatment but not in colonic epithelial cell CD98-overexpressing mice. Interestingly, the expression of potential miRNA target genes affected intestinal epithelial cells that overexpress CD98 and cell types that did not overexpress CD98 but were in close proximity to CD98-overexpressing intestinal epithelial cells. Taken together, these observations show that the combination of an inflammatory context and intestinal epithelial cell expression of CD98 affects the regulation of miRNA expression in colonic epithelial and immune cells. This is new evidence that protein expression modulates miRNA expression and suggests the existence of regulatory crosstalk between proteins and miRNAs in diseases such as colitis.

19 DIET-INDUCED OBESITY UNIQUELY REGULATES GLUCOSE AND NACL ABSORPTION IN SPRAGUE DAWLEY RAT SMALL INTESTINAL EPITHELIAL CELLS.

2021 ◽  
Vol 160 (6) ◽  
pp. S-3
Author(s):  
Balasubramanian Palaniappan ◽  
Subha Arthur ◽  
Raja Singh Paulraj ◽  
Shanmuga Sundaram ◽  
Niraj Nepal ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial ◽  
Sprague Dawley ◽  
Nacl Absorption ◽  
Diet Induced Obesity ◽  
Sprague Dawley Rat ◽  
Small Intestinal

scholarly journals Gut Microbiota Dysbiosis in Systemic Lupus Erythematosus: Novel Insights into Mechanisms and Promising Therapeutic Strategies

2021 ◽  
Vol 12 ◽  
Author(s):  
Quanren Pan ◽  
Fengbiao Guo ◽  
Yanyan Huang ◽  
Aifen Li ◽  
Shuxian Chen ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Epithelial Cells ◽  
Gut Microbiota ◽  
Lupus Erythematosus ◽  
Intestinal Epithelial Cells ◽  
Therapeutic Strategies ◽  
Oral Antibiotic ◽  
Intestinal Epithelial ◽  
Systemic Lupus ◽  
Gut Microbiota Dysbiosis

Systemic lupus erythematosus (SLE) is a chronic autoimmune disease that was traditionally thought to be closely related to genetic and environmental risk factors. Although treatment options for SLE with hormones, immunosuppressants, and biologic drugs are now available, the rates of clinical response and functional remission of these drugs are still not satisfactory. Currently, emerging evidence suggests that gut microbiota dysbiosis may play crucial roles in the occurrence and development of SLE, and manipulation of targeting the gut microbiota holds great promises for the successful treatment of SLE. The possible mechanisms of gut microbiota dysbiosis in SLE have not yet been well identified to date, although they may include molecular mimicry, impaired intestinal barrier function and leaky gut, bacterial biofilms, intestinal specific pathogen infection, gender bias, intestinal epithelial cells autophagy, and extracellular vesicles and microRNAs. Potential therapies for modulating gut microbiota in SLE include oral antibiotic therapy, fecal microbiota transplantation, glucocorticoid therapy, regulation of intestinal epithelial cells autophagy, extracellular vesicle-derived miRNA therapy, mesenchymal stem cell therapy, and vaccination. This review summarizes novel insights into the mechanisms of microbiota dysbiosis in SLE and promising therapeutic strategies, which may help improve our understanding of the pathogenesis of SLE and provide novel therapies for SLE.

scholarly journals Hypoxic environment promotes barrier formation in human intestinal epithelial cells through regulation of miRNA-320a expression

2018 ◽  
Author(s):  
Stephanie Muenchau ◽  
Rosalie Deutsch ◽  
Thomas Hielscher ◽  
Nora Heber ◽  
Beate Niesler ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Mirna Expression ◽  
Barrier Function ◽  
Intestinal Epithelial Cells ◽  
Hypoxia Inducible Factor ◽  
Intestinal Epithelial ◽  
Low Oxygen ◽  
Direct Role ◽  
Hypoxic Conditions ◽  
Barrier Formation

AbstractIntestinal epithelial cells (IECs) are exposed to the low-oxygen environment present in the lumen of the gut. These hypoxic conditions are on one hand fundamental for the survival of the commensal microbiota, and on the other hand, favor the formation of a selective semipermeable barrier allowing IECs to transport essential nutrients/water while keeping the sterile internal compartments separated from the lumen containing commensals. The hypoxia-inducible factor (HIF) complex, which allows cells to respond and adapt to fluctuations in oxygen levels, has been described as a key regulator in maintaining IEC barrier function by regulating their tight junction integrity. In this study, we sought to better evaluate the mechanisms by which low oxygen conditions impact the barrier function of human IECs. By profiling miRNA expression in IECs under hypoxia, we identified miRNA-320a as a novel barrier formation regulator. Using pharmacological inhibitors and short hairpin RNA-mediated silencing we could demonstrate that expression of this miRNA was HIF-dependent. Importantly, using over-expression and knock-down approaches of miRNA-320a we could confirm its direct role in the regulation of barrier functions in human IECs. These results reveal an important link between miRNA expression and barrier integrity, providing a novel insight into mechanisms of hypoxia-driven epithelial homeostasis.

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