Synergistic effect of tumor necrosis factor-alpha and interferon-gamma on enterocyte shedding of syndecan-1 and associated decreases in internalization of Listeria monocytogenes and Staphylococcus aureus

Michelle J. Henry-Stanley, Bin Zhang, Stanley L. Erlandsen, Carol L. Wells

Research output: Contribution to journalArticlepeer-review

18 Scopus citations

Abstract

Syndecan-1 is a heparan sulfate proteoglycan expressed on epithelia, and its ectodomain can be shed into the extracellular milieu, affecting a variety of cellular functions. Using two bacteria known to react with heparan sulfate, Listeria monocytogenes and Staphylococcus aureus, experiments were designed to clarify the effect of syndecan-1 shedding on bacterial internalization by human HT-29 enterocytes. Mature enterocytes were incubated with tumor necrosis factor (TNF)-α and/or interferon (IFN)-γ for 16 h prior to addition of bacteria. These cytokines acted synergistically to decrease syndecan-1 expression, assessed by visual observations of syndecan-1 expression on enterocytes using immunohistochemistry and a monoclonal antibody to the syndecan-1 core protein, by quantifying this fluorescent intensity, and by quantifying the concentration of shed syndecan-1 using an enzyme-linked immunoabsorbent assay. Neither IFN-γ nor TNF-α alone had a noticeable effect on L. monocytogenes internalization, but a mixture of both cytokines resulted in decreased (P < 0.01) internalization. Enterocyte preincubation with TNF-α alone, and with both cytokines, was associated with decreased S. aureus internalization, at P < 0.05 and P < 0.01, respectively. Thus, TNF-α and IFN-γ acted synergistically to shed syndecan-1 ectodomains from HT-29 enterocytes, and shedding was associated with decreased internalization of two pathogenic bacteria, suggesting that syndecan-1 shedding may modulate the pathogenesis of specific microbes.

Original languageEnglish (US)
Pages (from-to)252-259
Number of pages8
JournalCytokine
Volume34
Issue number5-6
DOIs
StatePublished - Jun 1 2006

Keywords

  • Bacteria
  • Enterocyte
  • Interferon-γ
  • Syndecan-1
  • Tumor necrosis factor-α

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