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
2011 ◽  
Vol 1 (1) ◽  
pp. 16 ◽  
Author(s):  
S. Brijesh ◽  
Pundarikakshudu Tetali ◽  
Tannaz J. Birdi

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>


Author(s):  
Qiuju Wang ◽  
Xinyue Qiao ◽  
Mengzu Wang ◽  
Junfeng Jia ◽  
and Yizhe Cui

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.


2017 ◽  
Author(s):  
Shanshan Kong ◽  
Weiqiang Zhang

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.


2013 ◽  
Vol 80 (3) ◽  
pp. 928-934 ◽  
Author(s):  
Ghalia Kaci ◽  
Denise Goudercourt ◽  
Véronique Dennin ◽  
Bruno Pot ◽  
Joël Doré ◽  
...  

ABSTRACTStreptococcus salivariusis one of the first colonizers of the human oral cavity and gut after birth and therefore may contribute to the establishment of immune homeostasis and regulation of host inflammatory responses. The anti-inflammatory potential ofS. salivariuswas first evaluatedin vitroon human intestinal epithelial cells and human peripheral blood mononuclear cells. We show that liveS. salivariusstrains inhibitedin vitrothe activation of the NF-κB pathway on intestinal epithelial cells. We also demonstrate that the liveS. salivariusJIM8772 strain significantly inhibited inflammation in severe and moderate colitis mouse models. Thesein vitroandin vivoanti-inflammatory properties were not found with heat-killedS. salivarius, suggesting a protective response exclusively with metabolically active bacteria.


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