Induction of proinflammatory mediators requires activation of the TRAF, NIK, IKK and NF‐κB signal transduction pathway in astrocytes infected with Escherichia coli
- Authors
- Kim, Jung Mogg; Oh, Yukyoung; Lee, J. H.; Im, D. Y.; Kim, Yeoung-jeon; Youn, Jeehee; Lee, Chul-hoon; Son, Hyeon; Lee, Yongsung; Park, Joo-young; Choi, In Hong
- Issue Date
- May-2005
- Publisher
- Blackwell Publishing Inc.
- Keywords
- astrocytes; Escherichia coli; NF-kappa B; proinflammatory mediators
- Citation
- Clinical and Experimental Immunology, v.140, no.3, pp 450 - 460
- Pages
- 11
- Indexed
- SCIE
SCOPUS
- Journal Title
- Clinical and Experimental Immunology
- Volume
- 140
- Number
- 3
- Start Page
- 450
- End Page
- 460
- URI
- https://scholarworks.bwise.kr/erica/handle/2021.sw.erica/45939
- DOI
- 10.1111/j.1365-2249.2005.02804.x
- ISSN
- 0009-9104
1365-2249
- Abstract
- Escherichia coli is associated with inflammation in the brain. To investigate whether astrocytes are involved in E. coli-induced inflammation, we assessed the levels of expression of proinflammatory mediators produced by E. coli-infected astrocytes. E. coli infection in primary human astrocytes and cell lines increased expression of the CXC chemokine IL-8/GRO-alpha, the CC chemokine MCP-1, TNF-alpha, and iNOS. E. coli infection activated p65/p50 heterodimeric NF-kappa B and concurrently decreased the signals of I kappa B alpha. Blocking the NF-kappa B signals by I kappa B alpha-superrepressor-containing retrovirus or antisense p50 oligonucleotide transfection resulted in down-regulation of expression of the proinflammatory mediators. Furthermore, superrepressors of I kappa B alpha, I kappa B kinase (IKK) or NF-kappa B inducing kinase (NIK) inhibited the up-regulated expression of the downstream target genes of NF-kappa B such as IL-8 and MCP-1, and superrepressors of TNF receptor-associated factor (TRAF)2 and TRAF5 also inhibited expression of the E. coli-induced target genes of NF-kappa B. These results indicate that proinflammatory mediators such as the CXC chemokine IL-8/GRO-alpha, the CC chemokine MCP-1, TNF-alpha, and iNOS can be expressed in E. coli-infected astrocytes via an NF-kappa B pathway, suggesting that these mediators may contribute to inflammation in the brain, including infiltration of inflammatory cells.
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