Abstract:
:Escherichia coli O157:H7, a major Shiga toxin-producing pathogen, has a low infectious dose and causes serious illness in humans. The gastrointestinal tract of cattle is the primary reservoir of E. coli O157:H7, and thus, it is critical to eliminate or reduce E. coli O157:H7 gut colonization. Given that E. coli O157:H7 produces effectors that attenuate inflammatory signaling, we hypothesized that the host inflammatory response acts to perturb E. coli O157:H7 intestinal colonization. Tumor necrosis factor alpha (TNF-α) treatment of HT-29 cells resulted in increased expression of inflammatory cytokine interleukin 1β (IL-1β), IL-8, and TNF-α genes and increased IL-8 protein and resulted in decreased adhesion of E. coli O157:H7. Similarly, E. coli O157:H7 adhesion to cattle colonic explants was reduced by TNF-α treatment. Irrespective of the presence of E. coli O157:H7, TNF-α enhanced activation of p65, the key mediator of NF-κB inflammatory signaling, whereas E. coli O157:H7 infection suppressed this pathway by inhibiting p65 activation in HT-29 cells. To further explore the mechanisms linking the inflammatory response to attenuated E. coli O157:H7 adhesion, mucin 2 (MUC2) expression was analyzed, considering that the intestinal mucus layer is the first defense against enteric pathogens and MUC2 is the major secretory mucin in the intestine. MUC2 expression in HT-29 cells was increased by TNF-α treatment and by E. coli O157:H7 infection. However, reducing mucin expression by blocking mitogen-activated protein kinase (MAPK) extracellular signal-regulated protein kinases 1/2 (ERK1/2) and/or phosphatidylinositol 3-kinase (PI3K)/Akt signaling increased E. coli O157:H7 adherence to HT-29 cells. These data suggest that the inflammatory cytokine response acts to protect host epithelial cells against E. coli O157:H7 colonization, at least in part, by promoting mucin production.
journal_name
Infect Immunjournal_title
Infection and immunityauthors
Xue Y,Zhang H,Wang H,Hu J,Du M,Zhu MJdoi
10.1128/IAI.01589-13subject
Has Abstractpub_date
2014-05-01 00:00:00pages
1921-30issue
5eissn
0019-9567issn
1098-5522pii
IAI.01589-13journal_volume
82pub_type
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journal_title:Infection and immunity
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doi:10.1128/IAI.31.1.358-361.1981
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doi:10.1128/IAI.54.2.465-471.1986
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doi:10.1128/IAI.54.1.85-89.1986
更新日期:1986-10-01 00:00:00
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pub_type: 杂志文章
doi:10.1128/IAI.44.2.394-400.1984
更新日期:1984-05-01 00:00:00
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journal_title:Infection and immunity
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doi:10.1128/IAI.31.1.144-150.1981
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journal_title:Infection and immunity
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journal_title:Infection and immunity
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