We found a match
Your institution may have rights to this item. Sign in to continue.
- Title
Induction of proinflammatory mediators requires activation of the TRAF, NIK, IKK and NF-κB signal transduction pathway in astrocytes infected withEscherichia coli.
- Authors
Kim, J. M.; Oh, Y.-K.; Lee, J. H.; Im, D. Y.; Kim, Y.-J.; Youn, J.; Lee, C.-H.; Son, H.; Lee, Y.-S.; Park, J. Y.; Choi, I.-H.
- Abstract
Escherichia coliis associated with inflammation in the brain. To investigate whether astrocytes are involved inE. coil-induced inflammation, we assessed the levels of expression of proinflammatory mediators produced byE. coli-infected astrocytes.E. coliinfection in primary human astrocytes and cell lines increased expression of the CXC chemokine IL-8/GRO-α, the CC chemokine MCP-1, TNF-α, and iNOS.E. coliinfection activated p65/p50 heterodimeric NF-κB and concurrently decreased the signals of IκBα. Blocking the NF-κB signals by IκBα-superrepressor-containing retrovirus or antisense p50 oligonucleotide transfection resulted in down-regulation of expression of the proinflammatory mediators. Furthermore, superrepressors of IκBα, IκB kinase (IKK) or NF-κB inducing kinase (NIK) inhibited the up-regulated expression of the downstream target genes of NF-κB such as IL-8 and MCP-1, and superrepressors of TNF receptor-associated factor (TRAF)2 and TRAF5 also inhibited expression of theE. coli-induced target genes of NF-κB. These results indicate that proinflammatory mediators such as the CXC chemokine IL-8/GRO-α, the CC chemokine MCP-1, TNF-α, and iNOS can be expressed inE. coli-infected astrocytes via an NF-κB pathway, suggesting that these mediators may contribute to inflammation in the brain, including infiltration of inflammatory cells.
- Subjects
ASTROCYTES; NEUROGLIA; INFLAMMATION; ESCHERICHIA coli; CELL lines; CHEMOKINES
- Publication
Clinical & Experimental Immunology, 2005, Vol 140, Issue 3, p450
- ISSN
0009-9104
- Publication type
Article
- DOI
10.1111/j.1365-2249.2005.02804.x