TY - JOUR
T1 - 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
AU - Henry-Stanley, Michelle J.
AU - Zhang, Bin
AU - Erlandsen, Stanley L.
AU - Wells, Carol L.
N1 - Funding Information:
This work was supported by Public Health Service Grant GM 066751 from the National Institutes of Health, USA.
PY - 2006/6
Y1 - 2006/6
N2 - 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.
AB - 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.
KW - Bacteria
KW - Enterocyte
KW - Interferon-γ
KW - Syndecan-1
KW - Tumor necrosis factor-α
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U2 - 10.1016/j.cyto.2006.05.008
DO - 10.1016/j.cyto.2006.05.008
M3 - Article
C2 - 16884912
AN - SCOPUS:33747113334
SN - 1043-4666
VL - 34
SP - 252
EP - 259
JO - Cytokine
JF - Cytokine
IS - 5-6
ER -