Expression Pattern Analysis of Antiviral Genes and Inflammatory Cytokines in PEDV-Infected Porcine Intestinal Epithelial Cells

Background Peroxiredoxin 1 (PRDX1), a protein with anti-inflammatory and anti-apoptotic properties, shows elevated expression in ulcerative colitis (UC). However, PRDX1's specific role in UC is poorly understood. Methods UC was induced in rats using dextran sulfate sodium (DSS). In vivo RNA interference was used to silence the PRDX1 expression. PRDX1 expression levels and the inflammatory cytokines tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, transforming growth factor (TGF)-β and interferon (IFN)-γ in tissues were assessed by real-time quantitative polymerase chain reaction and western blotting. Colonic injury was assessed by hematoxylin–eosin staining. ELISA was used to assess levels of the inflammatory cytokines TNF-α, IL-1β and IL-6 in colon tissues. Apoptosis of intestinal epithelial cells was assessed by terminal deoxynucleotidyl transferase dUTP nick end labeling, and expression of the apoptotic proteins bcl-2, Bax, cleaved caspase-3 and caspase-3 was assessed by western blotting. Results PRDX1 expression was significantly increased in rats with DSS-induced UC. Silencing of PRDX1 expression improved colon injury in rats with DSS-induced UC. In addition, silencing of PRDX1 expression inhibited inflammatory responses and apoptosis of intestinal epithelial cells in rats with DSS-induced UC. Conclusions Silencing of PRDX1 expression can ameliorate colon injury in rats with DSS-induced UC.

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Intestinal Bacteroides Modulates Systemic Inflammation and the Microbial Ecology in a Mouse Model of CF: Evidence for Propionate and other Short Chain Fatty Acids Reducing Systemic Inflammatory Cytokines

10.1101/2022.01.05.475125 ◽

2022 ◽

Author(s):

Courtney Price ◽

Rebecca Valls ◽

Alexis Ramsey ◽

Nicole Loeven ◽

Jane Jones ◽

...

Keyword(s):

Epithelial Cells ◽

Inflammatory Response ◽

Inflammatory Cytokines ◽

Relative Abundance ◽

Intestinal Epithelial Cells ◽

Short Chain Fatty Acids ◽

Short Chain ◽

Intestinal Microbiome ◽

Dependent Manner ◽

Intestinal Epithelial

Persons with cystic fibrosis, starting in early life, have intestinal microbiome dysbiosis characterized in part by a decreased relative abundance of the genus Bacteroides. Bacteroides is a major producer of the intestinal short chain fatty acid (SCFA) propionate. We demonstrate here that CFTR-/- Caco-2 intestinal epithelial cells are responsive to the anti-inflammatory effects of propionate. Furthermore, Bacteroides isolates inhibit the IL-1β-induced inflammatory response of CFTR-/- Caco-2 intestinal epithelial cells and do so in a propionate-dependent manner. Bacteroides isolates also produce low levels of butyrate; this SCFA is positively correlated with inhibition of the inflammatory response. Finally, the introduction of Bacteroides-supplemented stool from infants with CF into the gut of CftrF508del mice results in an increase in propionate in the stool as well as the reduction in several systemic pro-inflammatory cytokines. Bacteroides supplementation also reduced the fecal relative abundance of E. coli, indicating a potential interaction between these two microbes, consistent with previous clinical studies. Together, our data indicate the important role of Bacteroides and Bacteroides-derived propionate in the context of the developing microbiome in infants and children with CF, which could help explain the observed gut-lung axis in CF.

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Aichi Virus Induces Antiviral Host Defense in Primary Murine Intestinal Epithelial Cells

Viruses ◽

10.3390/v11080763 ◽

2019 ◽

Vol 11 (8) ◽

pp. 763

Author(s):

Yun-Te Chang ◽

Ming-Hsiang Kung ◽

Thung-Hsien Hsu ◽

Wan-Ting Hung ◽

Yao-Shen Chen ◽

...

Keyword(s):

Epithelial Cells ◽

Inflammatory Cytokines ◽

Host Defense ◽

Intestinal Epithelial Cells ◽

Rna Virus ◽

Human Colon ◽

Aichi Virus ◽

Type I ◽

Intestinal Epithelial ◽

Primary Mouse

The picornavirus Aichi virus (AiV) is a non-enveloped RNA virus that causes acute gastroenteritis symptoms, such as diarrhea, abdominal pain, nausea, vomiting, and fever. Antiviral host defense involves the fast response of type I interferon (IFN) and the secretion of inflammatory cytokines against pathogens. However, the intestinal inflammatory and antiviral response to AiV infection is poorly understood. This study evaluated the antiviral activity of intestinal epithelial cells (IECs), which form a single-cell layer separating the bowel wall from pathogens. Isolated primary mouse IECs were subjected to AiV infection and virion production, inducing the mRNA expression of type I/type III IFNs and inflammatory cytokines. The mechanism involved induced the expression of phospho-IFN regulatory factor 3 and mitochondrial antiviral-signaling protein of type I IFN signaling. These findings were also observed in AiV-infected human colon carcinoma cells. In summary, a viral productive and pathogenic infection of AiV in primary murine IECs is validated.

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Lactoferrin downregulates pro-inflammatory cytokines upexpressed in intestinal epithelial cells infected with invasive or noninvasive Escherichia coli strainsThis paper is one of a selection of papers published in this Special Issue, entitled 7th International Conference on Lactoferrin: Structure, Function, and Applications, and has undergone the Journal’s usual peer review process.

Biochemistry and Cell Biology ◽

10.1139/o06-039 ◽

2006 ◽

Vol 84 (3) ◽

pp. 351-357 ◽

Cited By ~ 56

Author(s):

Francesca Berlutti ◽

Serena Schippa ◽

Clara Morea ◽

Serena Sarli ◽

Brunella Perfetto ◽

...

Keyword(s):

Escherichia Coli ◽

Epithelial Cells ◽

Inflammatory Cytokines ◽

Pathogenic Bacteria ◽

Intestinal Epithelial Cells ◽

Peer Review Process ◽

Bovine Lactoferrin ◽

Intestinal Epithelial ◽

E Coli ◽

Pro Inflammatory Cytokines

Intestinal epithelial cells are able to differentially interact with commensal or pathogenic microorganisms, triggering a physiological or destructive inflammation, respectively. To mimic commensal–enteroinvasive bacteria–host cell interaction, we infected Caco-2 cells with noninvasive Escherichia coli HB101 and with recombinant invasive E. coli HB101(pRI203). Using DNA microarray mRNA profiling and ELISA assays, we studied the expression of several cytokine and cytokine-related genes in infected Caco-2 cells in the absence or presence of bovine lactoferrin (bLf). Infection of Caco-2 cells with the noninvasive strain induced a slight increase in the expression of interleukin 8 (IL-8), whereas infection with invasive E. coli HB101(pRI203) induced a significant increase in the expression of IL-8 as well as other pro-inflammatory cytokines. The addition of bLf, in native- or holo-form, did not influence expression of cytokine genes by uninfected Caco-2 cells, but it decreased expression of IL-8 by cells infected with E.coli HB101. Moreover, except for IL-8, bLfs dramatically downregulated pro-inflammatory cytokines upexpressed by Caco-2 cells infected with the invasive strain. Although IL-8 was decreased by bLfs, it remained upregulated, suggesting that it could be a signal of persistence of intracellular bacteria. The bLf ability to reduce expression of some pro-inflammatory cytokines, which appears independent of its iron saturation, might represent an important natural mechanism in regulating epithelial cell responses to pathogenic bacteria and in limiting cell damage and the spread of infections.

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Protective effects of baicalin on LPS-induced injury in intestinal epithelial cells and intercellular tight junctions

Canadian Journal of Physiology and Pharmacology ◽

10.1139/cjpp-2014-0262 ◽

2015 ◽

Vol 93 (4) ◽

pp. 233-237 ◽

Cited By ~ 24

Author(s):

Jian Chen ◽

Ren Zhang ◽

Jian Wang ◽

Peng Yu ◽

Quan Liu ◽

...

Keyword(s):

Epithelial Cells ◽

Protein Expression ◽

Tight Junctions ◽

Inflammatory Cytokines ◽

Intestinal Epithelial Cells ◽

Expression Level ◽

Protective Effects ◽

Intestinal Epithelial ◽

Tnf Α ◽

Mrna And Protein Expression

Aims: To investigate the protective effects and mechanisms of baicalin on lipopolysaccharide (LPS)-induced injury in intestinal epithelial cells and intercellular tight junctions. Methods: IEC-6 cells were stimulated with LPS (1.0 μg/mL), with or without baicalin, for 24 h. The levels of the inflammatory cytokines interleukin (IL)-6 and tumor necrosis factor (TNF)-α were determined using ELISA. Quantitative real-time PCR was used for determining the mRNA expression level of claudin-3, occludin, and ZO-1; Western blot and immunofluorescence analysis were used for analyzing the expression level and the distribution patterns of ZO-1 protein. Results: Pretreatment with baicalin (10.0 μg/mL) improved LPS-stimulated cell viability and repressed IL-6 and TNF-α levels. In addition, pretreatment with baicalin up-regulated mRNA and protein expression levels of ZO-1 and kept the protein intact in IEC-6 cells injured with LPS. Conclusion: Baicalin has the capacity to protect IEC-6 cells and the intercellular tight junctions from LPS-induced injury. The mechanisms may be associated with inhibiting the production of inflammatory cytokines, and up-regulating the mRNA and protein expression of ZO-1.

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