Induction of interleukin-8 production via nuclear factor-κB activation in human intestinal epithelial cells infected with Vibrio vulnificus

B. C. Lee, S. H. Kim, S. H. Choi, Tae Sung Kim

Research output: Contribution to journalArticle

20 Citations (Scopus)

Abstract

Vibrio vulnificus, a Gram-negative estuarine bacterium, is a causative agent of food-borne diseases, such as life-threatening septicaemia and wound infection disease. V. vulnificus penetrating into the epithelial barrier stimulates an inflammatory response in the adjacent mucosa. Therefore, interaction between V. vulnificus and epithelial cells is important for understanding of both the immunology of mucosal surfaces and V. vulnificus. In this study, we investigated the effect and action mechanism of V. vulnificus infection on production of interleukin (IL)-8, a proinflammatory cytokine, in human intestinal epithelial INT-407 cells. V. vulnificus infection significantly induced IL-8 production in a time- and multiplicity of infection (MOI)-dependent manner, as determined by human IL-8 enzyme-linked immunosorbent assay (ELISA). In addition, V. vulnificus infection significantly increased IL-8 mRNA levels in INT-407 cells, indicating that the increased IL-8 production by V. vulnificus occurred at the transcriptional level. V. vulnificus infection also enhanced IL-8 gene promoter activity in INT-407 cells transiently transfected with IL-8 promoter constructs, but this effect was impaired in INT-407 cells transfected with IL-8 promoter constructs deleted or mutated of a κB site. V. vulnificus infection increased the nuclear factor-kappaB (NF-κB) binding activity to a κB site and the degradation of IκB-α protein in a time- and a MOI-dependent manner. Furthermore, BAY11-7082, an inhibitor of NF-κB activation, significantly reduced the IL-8 production, NF-κB binding activity and IκB-α degradation induced by V. vulnificus infection. Taken together, these results indicate clearly that V. vulnificus infection significantly induces IL-8 production in human intestinal epithelial cells via NF-κB activation.

Original languageEnglish
Pages (from-to)506-515
Number of pages10
JournalImmunology
Volume115
Issue number4
DOIs
Publication statusPublished - 2005 Aug 1
Externally publishedYes

Fingerprint

Vibrio vulnificus
Interleukin-8
Epithelial Cells
Foodborne Diseases
Wound Infection
Infection
Vibrio vulnificus infection
Allergy and Immunology
Gram-Negative Bacteria
Proteolysis
Sepsis
Mucous Membrane
Enzyme-Linked Immunosorbent Assay

Keywords

  • Epithelial cell
  • Interleukin-8
  • Nuclear factor-κB
  • Vibrio vulnificus

ASJC Scopus subject areas

  • Immunology

Cite this

Induction of interleukin-8 production via nuclear factor-κB activation in human intestinal epithelial cells infected with Vibrio vulnificus. / Lee, B. C.; Kim, S. H.; Choi, S. H.; Kim, Tae Sung.

In: Immunology, Vol. 115, No. 4, 01.08.2005, p. 506-515.

Research output: Contribution to journalArticle

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abstract = "Vibrio vulnificus, a Gram-negative estuarine bacterium, is a causative agent of food-borne diseases, such as life-threatening septicaemia and wound infection disease. V. vulnificus penetrating into the epithelial barrier stimulates an inflammatory response in the adjacent mucosa. Therefore, interaction between V. vulnificus and epithelial cells is important for understanding of both the immunology of mucosal surfaces and V. vulnificus. In this study, we investigated the effect and action mechanism of V. vulnificus infection on production of interleukin (IL)-8, a proinflammatory cytokine, in human intestinal epithelial INT-407 cells. V. vulnificus infection significantly induced IL-8 production in a time- and multiplicity of infection (MOI)-dependent manner, as determined by human IL-8 enzyme-linked immunosorbent assay (ELISA). In addition, V. vulnificus infection significantly increased IL-8 mRNA levels in INT-407 cells, indicating that the increased IL-8 production by V. vulnificus occurred at the transcriptional level. V. vulnificus infection also enhanced IL-8 gene promoter activity in INT-407 cells transiently transfected with IL-8 promoter constructs, but this effect was impaired in INT-407 cells transfected with IL-8 promoter constructs deleted or mutated of a κB site. V. vulnificus infection increased the nuclear factor-kappaB (NF-κB) binding activity to a κB site and the degradation of IκB-α protein in a time- and a MOI-dependent manner. Furthermore, BAY11-7082, an inhibitor of NF-κB activation, significantly reduced the IL-8 production, NF-κB binding activity and IκB-α degradation induced by V. vulnificus infection. Taken together, these results indicate clearly that V. vulnificus infection significantly induces IL-8 production in human intestinal epithelial cells via NF-κB activation.",
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