Interferon (IFN)-Γ regulated production of chemoattractants specific for CD4+ memory T cells by human intestinal epithelial cells

2000 ◽  
Vol 118 (4) ◽  
pp. A672
Author(s):  
Michael B. Dwinell ◽  
Norbert Luegering ◽  
Lars Eckmann ◽  
Martin F. Kagnoff
Keyword(s):  
T Cells ◽  
Epithelial Cells ◽  
Memory T Cells ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial ◽  
Human Intestinal Epithelial Cells ◽  
Ifn Γ

TNF-α and IFN-γ regulate the expression of the NOD2 (CARD15) gene in human intestinal epithelial cells

2003 ◽  
Vol 124 (4) ◽  
pp. 1001-1009 ◽  
Author(s):  
Philip Rosenstiel ◽  
Massimo Fantini ◽  
Karen Bräutigam ◽  
Tanja Kühbacher ◽  
Georg H. Waetzig ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial ◽  
Human Intestinal Epithelial Cells ◽  
Tnf Α ◽  
Ifn Γ ◽  
Card15 Gene

TNF-α and IFN-γ regulate the expression of the NOD2 (CARD15) gene in human intestinal epithelial cells

2003 ◽  
Vol 124 (4) ◽  
pp. A111 ◽  
Author(s):  
Philip Rosenstiel ◽  
Massimo Fantini ◽  
Karen Braeutigam ◽  
Georg Waetzig ◽  
Tanja Kuehbacher ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial ◽  
Human Intestinal Epithelial Cells ◽  
Tnf Α ◽  
Ifn Γ ◽  
Card15 Gene

scholarly journals Salmonella entericaSerovar Typhimurium Increases Functional PD-L1 Synergistically with Gamma Interferon in Intestinal Epithelial Cells viaSalmonellaPathogenicity Island 2

2018 ◽  
Vol 86 (5) ◽  
pp. e00674-17 ◽  
Author(s):  
J. M. Sahler ◽  
C. R. Eade ◽  
C. Altier ◽  
J. C. March
Keyword(s):  
T Cells ◽  
Epithelial Cells ◽  
Host Cell ◽  
Immune Evasion ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial ◽  
Activated T Cells ◽  
Content Type ◽  
Ifn Γ ◽  
First Time

ABSTRACTNontyphoidal serovars ofSalmonella entericaare pathogenic bacteria that are common causes of food poisoning. WhereasSalmonellamechanisms of host cell invasion, inflammation, and pathogenesis are mostly well established, a new possible mechanism of immune evasion is being uncovered. Programmed death ligand 1 (PD-L1) is an immunosuppressive membrane protein that binds to activated T cells via their PD-1 receptor and thereby halts their activation. PD-L1 expression plays an essential role in the immunological tolerance of self-antigens but is also exploited for immune evasion by pathogen-infected cells and cancer cells. Here, we show for the first time thatSalmonellainfection of intestinal epithelial cells causes the induction of PD-L1. The increased expression of PD-L1 throughSalmonellainfection was seen in both human and rat intestinal epithelial cell lines. We determined that cellular invasion by the bacteria is necessary for PD-L1 induction, potentially indicating thatSalmonellastrains are delivering mediators from inside the host cell that trigger the increased PD-L1 expression. Using knockout mutants, we determined that this effect largely originates from theSalmonellapathogenicity island 2. We also show for the first time in any cell type thatSalmonellacombined with gamma interferon (IFN-γ) causes a synergistic induction of PD-L1. Finally, we show thatSalmonellaplus IFN-γ induction of PD-L1 decreased the cytokine production of activated T cells. UnderstandingSalmonellaimmune evasion strategies could generate new therapeutic targets and help to manipulate PD-L1 expression in other diseases.

Modulation of complement C3, C4, and factor B production in human intestinal epithelial cells: differential effects of TNF-α, IFN-γ, and IL-4

1995 ◽  
Vol 2 (4) ◽  
pp. 251-259 ◽  
Author(s):  
Akira Andoh ◽  
Yoshihide Fujiyama ◽  
Kenichi Sumiyoshi ◽  
Keiko Hodohara ◽  
Okabe Hidetoshi ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Intestinal Epithelial Cells ◽  
Complement C3 ◽  
Intestinal Epithelial ◽  
Factor B ◽  
Differential Effects ◽  
Human Intestinal Epithelial Cells ◽  
Tnf Α ◽  
Ifn Γ

scholarly journals Interferon Regulatory Factor 1 (IRF-1) and IRF-2 Distinctively Up-Regulate Gene Expression and Production of Interleukin-7 in Human Intestinal Epithelial Cells

2004 ◽  
Vol 24 (14) ◽  
pp. 6298-6310 ◽  
Author(s):  
Shigeru Oshima ◽  
Tetsuya Nakamura ◽  
Shin Namiki ◽  
Eriko Okada ◽  
Kiichiro Tsuchiya ◽  
...  
Keyword(s):  
Gene Expression ◽  
Epithelial Cells ◽  
Intestinal Mucosa ◽  
Intestinal Epithelial Cells ◽  
Core Promoter ◽  
Expression Patterns ◽  
Intestinal Epithelial ◽  
Regulatory Factor ◽  
Human Intestinal Epithelial Cells ◽  
Ifn Γ

ABSTRACT Intestinal epithelial cell-derived interleukin (IL)-7 functions as a pleiotropic and nonredundant cytokine in the human intestinal mucosa; however, the molecular basis of its production has remained totally unknown. We here showed that human intestinal epithelial cells both constitutively and when induced by gamma interferon (IFN-γ) produced IL-7, while several other factors we tested had no effect. Transcriptional regulation via an IFN regulatory factor element (IRF-E) on the 5′ flanking region, which lacks canonical core promoter sequences, was pivotal for both modes of IL-7 expression. IRF-1 and IRF-2, the latter of which is generally known as a transcriptional repressor, were shown to interact with IRF-E and transactivate IL-7 gene expression in an IFN-γ-inducible and constitutive manner, respectively. Indeed, tetracycline-inducible expression experiments revealed that both of these IRF proteins up-regulated IL-7 protein production, and their exclusive roles were further confirmed by small interfering RNA-mediated gene silencing systems. Moreover, these IRFs displayed distinct properties concerning the profile of IL-7 transcripts upon activation and expression patterns within human colonic epithelial tissues. These results suggest that the functional interplay between IRF-1 and IRF-2 serves as an elaborate and cooperative mechanism for timely as well as continuous regulation of IL-7 production that is essential for local immune regulation within human intestinal mucosa.

scholarly journals Anti-Inflammatory Effects of the Nicotinergic Peptides SLURP-1 and SLURP-2 on Human Intestinal Epithelial Cells and Immunocytes

2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Alex I. Chernyavsky ◽  
Valentin Galitovskiy ◽  
Igor B. Shchepotin ◽  
Sergei A. Grando
Keyword(s):  
T Cells ◽  
Epithelial Cells ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial ◽  
Therapeutic Modalities ◽  
Human Intestinal Epithelial Cells ◽  
Inflammatory Bowel ◽  
Anti Inflammatory ◽  
Contemporary Medicine ◽  
Inflammatory Action

A search for novel and more efficient therapeutic modalities of inflammatory bowel disease (IBD) is one of the most important tasks of contemporary medicine. The anti-inflammatory action of nicotine in IBD might be therapeutic, but its toxicity due to off-target and nonreceptor effects limited its use and prompted a search for nontoxic nicotinergic drugs. We tested the hypothesis that SLURP-1 and -2—the physiological nicotinergic substances produced by the human intestinal epithelial cells (IEC) and immunocytes—can mimic the anti-inflammatory effects of nicotine. We used human CCL-241 enterocytes, CCL-248 colonocytes, CCRF-CEM T-cells, and U937 macrophages. SLURP-1 diminished the TLR9-dependent secretion of IL-8 by CCL-241, and IFNγ-induced upregulation of ICAM-1 in both IEC types. rSLURP-2 inhibited IL-1β-induced secretion of IL-6 and TLR4- and TLR9-dependent induction of CXCL10 and IL-8, respectively, in CCL-241. rSLURP-1 decreased production of TNFαby T-cells, downregulated IL-1βand IL-6 secretion by macrophages, and moderately upregulated IL-10 production by both types of immunocytes. SLURP-2 downregulated TNFαand IFNγR in T-cells and reduced IL-6 production by macrophages. Combining both SLURPs amplified their anti-inflammatory effects. Learning the pharmacology of SLURP-1 and -2 actions on enterocytes, colonocytes, T cells, and macrophages may help develop novel effective treatments of IBD.

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