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Host Response and Inflammation

Escherichia coli K12 Upregulates Programmed Cell Death Ligand 1 (PD-L1) Expression in Gamma Interferon-Sensitized Intestinal Epithelial Cells via the NF-κB Pathway

Seul A. Lee, Yiming Wang, Fang Liu, Stephen M. Riordan, Lu Liu, Li Zhang
Manuela Raffatellu, Editor
Seul A. Lee
aSchool of Biotechnology and Biomolecular Sciences, University of New South Wales, Sydney, Australia
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Yiming Wang
aSchool of Biotechnology and Biomolecular Sciences, University of New South Wales, Sydney, Australia
bInfection & Immunity Theme, South Australian Health and Medical Research Institute, Adelaide, South Australia, Australia
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Fang Liu
aSchool of Biotechnology and Biomolecular Sciences, University of New South Wales, Sydney, Australia
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Stephen M. Riordan
cGastrointestinal and Liver Unit, Prince of Wales Hospital, University of New South Wales, Sydney, Australia
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Lu Liu
dSchool of Medical Sciences, University of New South Wales, Sydney, Australia
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Li Zhang
aSchool of Biotechnology and Biomolecular Sciences, University of New South Wales, Sydney, Australia
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Manuela Raffatellu
University of California San Diego School of Medicine
Roles: Editor
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DOI: 10.1128/IAI.00618-20
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ABSTRACT

Programmed cell death ligand-1 (PD-L1) is an immune checkpoint protein which is used by tumor cells for immune evasion. PD-L1 is upregulated in inflamed intestinal tissues. The intestinal tract is colonized by millions of bacteria, most of which are commensal bacterial species. We hypothesized that under inflammatory conditions, some commensal bacterial species contribute to increased PD-L1 expression in intestinal epithelium and examined this hypothesis. Human intestinal epithelial HT-29 cells with and without interferon (IFN)-γ sensitization were incubated with six strains of four enteric bacterial species. The mRNA and protein levels of PD-L1 in HT-29 cells were examined using quantitative real-time PCR and flow cytometry, respectively. The levels of interleukin (IL)-1β, IL-18, IL-6, IL-8, and tumor necrosis factor (TNF)-α secreted by HT-29 cells were measured using enzyme-linked immunosorbent assay. Apoptosis of HT-29 cells was measured using a caspase 3/7 assay. We found that Escherichia coli K12 significantly upregulated both PD-L1 mRNA and protein in IFN-γ-sensitized HT-29 cells. E. coli K12 induced the production of IL-8 in HT-29 cells, however, IL-8 did not affect HT-29 PD-L1 expression. Inhibition of the nuclear factor-kappa B pathway significantly reduced E. coli K12-induced PD-L1 expression in HT-29 cells. The other two E. coli strains and two enteric bacterial species did not significantly affect PD-L1 expression in HT-29 cells. Enterococcus faecalis significantly inhibited PD-L1 expression due to induction of cell death. Data from this study suggest that some gut bacterial species have the potential to affect immune function under inflammatory conditions via upregulating epithelial PD-L1 expression.

FOOTNOTES

    • Received 6 October 2020.
    • Accepted 6 October 2020.
    • Accepted manuscript posted online 12 October 2020.
  • Supplemental material is available online only.

  • Copyright © 2020 American Society for Microbiology.

All Rights Reserved.

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Escherichia coli K12 Upregulates Programmed Cell Death Ligand 1 (PD-L1) Expression in Gamma Interferon-Sensitized Intestinal Epithelial Cells via the NF-κB Pathway
Seul A. Lee, Yiming Wang, Fang Liu, Stephen M. Riordan, Lu Liu, Li Zhang
Infection and Immunity Dec 2020, 89 (1) e00618-20; DOI: 10.1128/IAI.00618-20

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Escherichia coli K12 Upregulates Programmed Cell Death Ligand 1 (PD-L1) Expression in Gamma Interferon-Sensitized Intestinal Epithelial Cells via the NF-κB Pathway
Seul A. Lee, Yiming Wang, Fang Liu, Stephen M. Riordan, Lu Liu, Li Zhang
Infection and Immunity Dec 2020, 89 (1) e00618-20; DOI: 10.1128/IAI.00618-20
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KEYWORDS

PD-L1
E. coli K12
inflammation
IFN-γ
intestinal epithelial cells

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