scholarly journals Colostrum whey down-regulates the expression of early and late inflammatory response genes induced byEscherichia coliandSalmonella entericaTyphimurium components in intestinal epithelial cells

2014 ◽  
Vol 113 (2) ◽  
pp. 200-211 ◽  
Author(s):  
M. Blais ◽  
M. Fortier ◽  
Y. Pouliot ◽  
S. F. Gauthier ◽  
Y. Boutin ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Transcriptional Activation ◽  
Inflammatory Responses ◽  
Intestinal Epithelial Cells ◽  
Colon Adenocarcinoma ◽  
Human Colon ◽  
Bovine Colostrum ◽  
Mucosal Barrier ◽  
Intestinal Epithelial ◽  
Inflammatory Genes

Pathogenic invasion byEscherichia coliandSalmonellaeremains a constant threat to the integrity of the intestinal epithelium and can rapidly induce inflammatory responses. At birth, colostrum consumption exerts numerous beneficial effects on the properties of intestinal epithelial cells and protects the gastrointestinal tract of newborns from pathogenic invasion. The present study aimed to investigate the effect of colostrum on the early and late inflammatory responses induced by pathogens. The short-term (2 h) and long-term (24 h) effects of exposure to heat-killed (HK)E. coliandSalmonella entericaTyphimurium on gene expression in the porcine intestinal epithelial cell (IPEC-J2) model were first evaluated by microarray and quantitative PCR analyses. Luciferase assays were performed using a NF-κB-luc reporter construct to investigate the effect of colostrum whey treatment on the activation of NF-κB induced by HK bacteria. Luciferase assays were also performed using NF-κB-luc, IL-8-luc and IL-6-luc reporter constructs in human colon adenocarcinoma Caco-2/15 cells exposed to dose–response stimulations with HK bacteria and colostrum whey. Bovine colostrum whey treatment decreased the expression of early and late inflammatory genes induced by HK bacteria in IPEC-J2, as well as the transcriptional activation of NF-κB-luc induced by HK bacteria. Unlike that with colostrum whey, treatment with other milk fractions failed to decrease the activation of NF-κB-luc induced by HK bacteria. Lastly, the reduction of the HK bacteria-induced activation of NF-κB-luc, IL-8-luc and IL-6-luc by colostrum whey was dose dependent. The results of the present study indicate that bovine colostrum may protect and preserve the integrity of the intestinal mucosal barrier in the host by controlling the expression levels of early and late inflammatory genes following invasion by enteric pathogens.

scholarly journals Study on effect of anti-diarrheal medicinal plants on enteropathogenic Escherichia coli induced interleukin-8 secretion by intestinal epithelial cells

2011 ◽  
Vol 1 (1) ◽  
pp. 16 ◽  
Author(s):  
S. Brijesh ◽  
Pundarikakshudu Tetali ◽  
Tannaz J. Birdi
Keyword(s):  
Escherichia Coli ◽  
Epithelial Cells ◽  
Medicinal Plants ◽  
Inflammatory Responses ◽  
Intestinal Epithelial Cells ◽  
Colon Adenocarcinoma ◽  
Cyperus Rotundus ◽  
Health Concern ◽  
Intestinal Epithelial ◽  
Infantile Diarrhea

Diarrhea is a major health concern in developing countries with enteropathogenic <em>Escherichia coli</em> (EPEC) being a leading cause of infantile diarrhea. Much of the pathology of EPEC infection is due to the inflammatory responses of infected intestinal epithelium through secretion of pro-inflammatory cytoki - nes such as interleukin (IL)-8. With medicinal plants gaining popularity as prospective antidiarrheal agents, we aimed to evaluate the effect of anti-diarrheal medicinal plants on secretion of IL-8 by epithelial cells in response to EPEC infection. The effect of the decoctions of four anti-diarrheal medicinal plants viz. <em>Aegle marmelos</em>, <em>Cyperus rotundus</em>, <em>Psidium guajava</em> and <em>Zingiber officinale</em> was studied on secretion of IL-8 by a human colon adenocarcinoma cell line, HT-29 infected with <em>E. coli </em>E2348/69. Two protocols were used viz. pre-incubation and post-incubation. The data obtained demonstrated that out of the four plants used, only <em>P. guajava</em> decreased secretion of IL-8 in the post-incubation protocol although in the pre-incubation protocol an increase was observed. A similar increase was seen with <em>C. rotundus</em> in the preincubation protocol. No effect on IL-8 secretion was observed with <em>A. marmelos</em> and <em>Z. officinale</em> in both protocols and with <em>C. rotundus </em>in the post-incubation protocol. The post-incubation protocol, in terms of clinical relevance, indicates the effect of the plant decoctions when used as treatment. Hence <em>P. guajava</em> may be effective in controlling the acute inflammatory response of the intestinal epithelial cells in response to EPEC infection.<p> </p>

scholarly journals Human milk oligosaccharides and non-digestible carbohydrates prevent adhesion of specific pathogens via modulating glycosylation or inflammatory genes in intestinal epithelial cells

2021 ◽  
Author(s):  
Chunli Kong ◽  
Martin Beukema ◽  
Min Wang ◽  
Bart J. de Haan ◽  
Paul de Vos
Keyword(s):  
Epithelial Cells ◽  
Human Milk ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial ◽  
Human Milk Oligosaccharides ◽  
Milk Oligosaccharides ◽  
Inflammatory Genes

Human milk oligosaccharides 2′-FL and pectins inhibited pathogen adhesion through modulating glycosylation and inflammatory genes in intestinal epithelial cells.

MiR-339 attenuates LPS-induced intestinal epithelial cells inflammatory responses and apoptosis by targeting TLR4

2020 ◽  
Vol 42 (9) ◽  
pp. 1097-1105 ◽  
Author(s):  
Meiying Xie ◽  
Lina Zhang ◽  
Luoye Li ◽  
Minhuan Fan ◽  
Lianjie Hou
Keyword(s):  
Epithelial Cells ◽  
Inflammatory Responses ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial

scholarly journals JunD enhances miR-29b levels transcriptionally and posttranscriptionally to inhibit proliferation of intestinal epithelial cells

2015 ◽  
Vol 308 (10) ◽  
pp. C813-C824 ◽  
Author(s):  
Tongtong Zou ◽  
Jaladanki N. Rao ◽  
Lan Liu ◽  
Lan Xiao ◽  
Hee Kyoung Chung ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Transcription Factor ◽  
Epithelial Cells ◽  
Transcriptional Activation ◽  
Binding Sites ◽  
Intestinal Epithelial Cells ◽  
Inhibitory Effect ◽  
Microrna Expression ◽  
Intestinal Epithelial ◽  
Gut Epithelium

Through its actions as component of the activating protein-1 (AP-1) transcription factor, JunD potently represses cell proliferation. Here we report a novel function of JunD in the regulation of microRNA expression in intestinal epithelial cells (IECs). Ectopically expressed JunD specifically increased the expression of primary and mature forms of miR-29b, whereas JunD silencing inhibited miR-29b expression. JunD directly interacted with the miR-29b1 promoter via AP-1-binding sites, whereas mutation of AP-1 sites from the miR-29b1 promoter prevented JunD-mediated transcriptional activation of the miR-29b1 gene. JunD also enhanced formation of the Drosha microprocessor complex, thus further promoting miR-29b biogenesis. Cellular polyamines were found to regulate miR-29b expression by altering JunD abundance, since the increase in miR-29b expression levels in polyamine-deficient cells was abolished by JunD silencing. In addition, miR-29b silencing prevented JunD-induced repression of IEC proliferation. Our findings indicate that JunD activates miR-29b by enhancing its transcription and processing, which contribute to the inhibitory effect of JunD on IEC growth and maintenance of gut epithelium homeostasis.

scholarly journals Geniposide, a Component of Gardenia Jasminoides Ellis, Inhibits NF-ĸb to Attenuate LPS-Induced Injury in Intestinal Epithelial Cells

2021 ◽  
Author(s):  
Qiuju Wang ◽  
Xinyue Qiao ◽  
Mengzu Wang ◽  
Junfeng Jia ◽  
and Yizhe Cui
Keyword(s):  
Epithelial Cells ◽  
Inflammatory Responses ◽  
Intestinal Epithelial Cells ◽  
Interleukin 1 ◽  
Inflammatory Factors ◽  
Enzyme Linked Immunosorbent Assay ◽  
Intestinal Epithelial ◽  
Migration Ability ◽  
Gardenia Jasminoides ◽  
Gardenia Jasminoides Ellis

The nuclear factor-ĸB (NF-ĸB) transcriptional system is a major effector pathway involved in inflammatory responses. Previous studies found that a Gardenia decoction (GD) inhibited the expression of NF-&kappa;B in a lipopolysaccharide (LPS)-stimulated mouse intestinal injury model. Herein, we hypothesized that geniposide (GE), a component of Gardenia jasminoides Ellis, also exerts anti-inflammatory effects and inhibits NF-ĸB activity in LPS-induced intestinal epithelial cells (IEC-6). IEC-6 cells were stimulated with LPS, following which the effects of GE on NF-ĸB signaling in the IEC-6 cells were examined by western blotting to detect IĸB phosphorylation/degradation. The expression of NF-&kappa;B was determined by immunofluorescence assay (IFA). Enzyme-linked immunosorbent assay (ELISA) was used to detect the inhibitory effect of GE on the release of tumor necrosis factor-&alpha; (TNF-&alpha;), interleukin-6 (IL-6) and interleukin-1&beta; (IL-1&beta;) activated by LPS in IEC-6 cells. In addition, the migration ability of IEC-6 cells was observed by the scratch method. These results showed that GE dose-dependently downregulated levels of the proinflammatory cytokines TNF-&alpha;, IL-6 and IL-1&beta; that had been upregulated by LPS and suppressed the phosphorylation of IĸB and NF-ĸB induced by LPS. Our findings indicated that GE could reduce LPS-induced NF-ĸB signaling and proinflammatory expression in IEC-6 cells and significantly enhance the migration of IEC-6 cells. Moreover, GE inhibited the expression of NF-&kappa;B, nuclear transfer, and transcriptional activity in IEC-6 cells. GE could block the synthesis of inflammatory factors of IEC-6 cells by inhibiting activation of the IĸB/NF-&kappa;B signaling pathway induced by LPS.

scholarly journals The function of macromolecular complex of CFTR-NHERF2-LPA2 in inflammatory responses of intestinal epithelial cells

2017 ◽  
Author(s):  
Shanshan Kong ◽  
Weiqiang Zhang
Keyword(s):  
Epithelial Cell ◽  
Epithelial Cells ◽  
Cell Line ◽  
Human Cell ◽  
Inflammatory Responses ◽  
Intestinal Epithelial Cells ◽  
Human Cell Line ◽  
Macromolecular Complex ◽  
Apical Surface ◽  
Intestinal Epithelial

AbstractCFTR is a cAMP-regulated chloride channel located in the apical surface of intestinal epithelial cells; where it forms a macromolecular complex with NHERF2 and LPA2. CFTR has been shown to play a role in the pathogenies of several types of secretory diarrheas. Inflammatory bowel disease (IBD) is a chronic condition of intestine characterized by severe inflammation and mucosal destruction, genetic analysis has shown that LPA contribute to IBD and patients of cystic fibrosis also display the phenotype of diarrhea. The purpose of this study is to investigate if this complex plays a role in the inflammatory responses of intestinal epithelium.We then explored the role of this complex in maintaining the integrity of tight junction and inflammatory responses in these cells. In vitro assays show that inhibiting CFTR or LPA2 in the intestinal epithelial cell could disrupt the epithelial cell junction, and reduce the TER of intestinal epithelial cells in both mouse and human cell line. EƯSA assay show that intriguing LPA2 through LPS or LPA can increase the secretion of IL-8, while inhibiting or SiRNA knockdown of LPA2 can decrease the secretion of IL-8 in mouse or human intestinal epithelial cells. The CFTR inhibitor can reduce the IL-8 secretion in both mouse and human cell line, the deletion of CFTR in mouse intestine does not affect the IL-8 level, but the knockdown of CFTR in human cell line reduced the IL-8 protein level. The deletion of CFTR in human also reduced the IL-8 mRNA level. This indicates the CFTR-LPA complex is necessary for the expression of IL-8.

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