Salmonella enterica Serovar Enteritidis Modulates Intestinal Epithelial miR-128 Levels to Decrease Macrophage Recruitment via Macrophage Colony-Stimulating Factor

Zhang, Tianfu; Yu, Junchuan; Zhang, Yaqin; Liu, Limin; Chen, Yuanyuan; Li, Donghai; Liu, Fenyong; Zhang, Chenyu; Gu, Hang; Zen, Ke

doi:10.1093/infdis/jiu006

Cited by 40 publications

(33 citation statements)

References 38 publications

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“…Recent studies have characterized deregulation of host miRNAs following infection with extracellular ( H. pylori ) (12), or intracellular ( Salmonella enterica ) (13), Gram-negative bacteria, as well as in the response to Gram-positive ( Listeria monocytogenes ) (14) and other pathogenic bacteria ( Mycobacterium (15) and Francisella species (16)).…”

Section: Introductionmentioning

confidence: 99%

The Effect of MicroRNA-375 Overexpression, an Inhibitor of Helicobacter pylori-Induced Carcinogenesis, on lncRNA SOX2OT

Shafiee

Aleyasin

Mowla

et al. 2016

Jundishapur J Microbiol

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BackgroundHelicobacter pylori is a major human pathogenic bacterium in gastric mucosa. Although the association between gastric cancer and H. pylori has been well-established, the molecular mechanisms underlying H. pylori-induced carcinogenesis are still under investigation. MicroRNAs (miRNAs) are small noncoding RNAs that modulate gene expression at the posttranscriptional level. Recently, studies have revealed that miRNAs are involved in immune response and host cell response to bacteria. Also, microRNA-375 (miR-375) is a key regulator of epithelial properties that are necessary for securing epithelium-immune system cross-talk. It has been recently reported that miR-375 acts as an inhibitor of H. pylori-induced gastric carcinogenesis. There are few reports on miRNA-mediated targeting long noncoding RNAs (lncRNAs).ObjectivesThis study aimed to examine the possible effect of miR-375 as an inhibitor of H. pylori-induced carcinogenesis on the expression of lncRNA SOX2 overlapping transcript (SOX2OT) and SOX2, a master regulator of pluripotency of cancer stem cells.Materials and MethodsIn a model cell line, NT-2 was transfected with the constructed expression vector pEGFP-C1 contained miR-375. The RNA isolations and cDNA synthesis were performed after 48 hours of transformation. Expression of miR-375 and SOX2OT and SOX2 were quantified using real-time polymerase chain reaction and compared with control cells transfected with pEGFP-C1-Mock clone. Cell cycle modification was also compared after transfections using the flow cytometry analysis.ResultsFollowing ectopic expression of miR-375, SOX2OT and SOX2 expression analysis revealed a significant decrease in their expression level (P < 0.05) in NT-2 cells compared to the control. Cell cycle analysis following ectopic expression of miR-375 in the NT-2 cells using propidium iodine staining revealed significant extension in sub-G1 cell cycle.ConclusionsThis is the first report to show down-regulation of SOX2OT and SOX2 following induced expression of miR-375. This finding may suggest expression regulation potential between different classes of ncRNAs, for example between miR-375 and SOX2OT. This data not only extends our understanding of possible ncRNA interactions in cancers but also may open novel investigation lines towards elucidation of molecular mechanisms controlling H. pylori inflammation and carcinogenesis.

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Section: Introductionmentioning

confidence: 99%

The Effect of MicroRNA-375 Overexpression, an Inhibitor of Helicobacter pylori-Induced Carcinogenesis, on lncRNA SOX2OT

Shafiee

Aleyasin

Mowla

et al. 2016

Jundishapur J Microbiol

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“…31 In human in-testinal epithelial HT29 cells, miRNA-128 level was strongly increased by infection with Salmonella enterica serovar enteritidis, and delivery of antimiRNA-128 antagomir into mice significantly increased macrophage recruitment and suppressed Salmonella infection. 32 These results suggest that miRNA-128 is involved in inflammatory response, and upregulation of miRNA-128 may reduce inflammatory responses. Nevertheless, to the best of the authors' knowledge, there has been no research that focused on the role of miRNA-128 in periodontitis or periodontopathogenassociated immune responses.…”

Section: Discussionmentioning

confidence: 90%

“…In mononuclear cells from Alzheimer disease, miRNA‐128 upregulation is suggested as the reason for the reduced amount of lysosomal cathepsins, and miRNA‐128 inhibition in monocytes improved amyloid β(1‐42) degrading ability 31 . In human intestinal epithelial HT29 cells, miRNA‐128 level was strongly increased by infection with Salmonella enterica serovar enteritidis , and delivery of antimiRNA‐128 antagomir into mice significantly increased macrophage recruitment and suppressed Salmonella infection 32 . These results suggest that miRNA‐128 is involved in inflammatory response, and upregulation of miRNA‐128 may reduce inflammatory responses.…”

Section: Discussionmentioning

confidence: 99%

Elevated MicroRNA‐128 in Periodontitis Mitigates Tumor Necrosis Factor‐α Response via p38 Signaling Pathway in Macrophages

Park

Song

et al. 2016

Journal of Periodontology

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“…Cimino et al [ 60 ] reported M-CSF is a direct target of miR-148b. Wang et al [ 61 ] identified M-CSF as a target gene of miR-214, and Zhang et al [ 62 ] reported M-CSF as a target of miR-128. The present study found miR-26a regulates M-CSF expression and recruitment of macrophages.…”

Section: Discussionmentioning

confidence: 99%

microRNA-26a suppresses recruitment of macrophages by down-regulating macrophage colony-stimulating factor expression through the PI3K/Akt pathway in hepatocellular carcinoma

Chai

Zhu

et al. 2015

J Hematol Oncol

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BackgroundmicroRNAs (miRNAs) have been reported to modulate macrophage colony-stimulating factor (M-CSF) and macrophages. The aim of this study was to find whether miR-26a can suppress M-CSF expression and the recruitment of macrophages.MethodsHepatocellular carcinoma (HCC) cell lines with decreased or increased expression of miR-26a were established in a previous study. M-CSF expression by tumor cells was measured by enzyme-linked immunosorbent assay, and cell migration assays were used to explore the effect of HCC cell lines on macrophage recruitment in vitro. Real-time PCR measured a panel of mRNAs expressed by macrophages. Xenograft models were used to observe tumor growth. Immunohistochemistry was conducted to study the relation between miR-26a expression and M-CSF expression and macrophage recruitment in patients with HCC.ResultsEctopic expression of miR-26a reduced expression of M-CSF. The conditioned medium (CM) from HepG2 cells that overexpressed miR-26a reduced the migration ability of THP-1 cells stimulated by phorbol myristate acetate (PMA) increased expression of interleukin (IL)-12b or IL-23 mRNA and decreased expression of chemokine (C-C motif) ligand (CCL)22, CCL17, and IL-10 mRNA, in comparison to the medium from the parental HepG2 cells. These effects could be interrupted by the PI3K/Akt pathway inhibitor LY294002. Ectopic expression of miR-26a in HCC cells suppressed tumor growth, M-CSF expression, and infiltration of macrophages in tumors. Similar results were also found when using HCCLM3 cells. Furthermore, the expression of miR-26a was inversely correlated with M-CSF expression and macrophage infiltration in tumor tissues from patients with HCC.ConclusionsmiR-26a expression reduced M-CSF expression and recruitment of macrophages in HCC.

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Salmonella enterica Serovar Enteritidis Modulates Intestinal Epithelial miR-128 Levels to Decrease Macrophage Recruitment via Macrophage Colony-Stimulating Factor

Abstract: Salmonella can upregulate intestinal epithelial miR-128 expression, which, in turn, decreases levels of epithelial cell-secreted M-CSF and M-CSF-induced macrophage recruitment.

Cited by 40 publications

References 38 publications

The Effect of MicroRNA-375 Overexpression, an Inhibitor of Helicobacter pylori-Induced Carcinogenesis, on lncRNA SOX2OT

The Effect of MicroRNA-375 Overexpression, an Inhibitor of Helicobacter pylori-Induced Carcinogenesis, on lncRNA SOX2OT

Elevated MicroRNA‐128 in Periodontitis Mitigates Tumor Necrosis Factor‐α Response via p38 Signaling Pathway in Macrophages

microRNA-26a suppresses recruitment of macrophages by down-regulating macrophage colony-stimulating factor expression through the PI3K/Akt pathway in hepatocellular carcinoma

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