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Induction of proinflammatory mediators requires activation of the TRAF, NIK, IKK and NF-κB signal transduction pathway in astrocytes infected withEscherichia coli.
- Source :
-
Clinical & Experimental Immunology . Jun2005, Vol. 140 Issue 3, p450-460. 11p. - Publication Year :
- 2005
-
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. [ABSTRACT FROM AUTHOR]
- Subjects :
- *ASTROCYTES
*NEUROGLIA
*INFLAMMATION
*ESCHERICHIA coli
*CELL lines
*CHEMOKINES
Subjects
Details
- Language :
- English
- ISSN :
- 00099104
- Volume :
- 140
- Issue :
- 3
- Database :
- Academic Search Index
- Journal :
- Clinical & Experimental Immunology
- Publication Type :
- Academic Journal
- Accession number :
- 17077819
- Full Text :
- https://doi.org/10.1111/j.1365-2249.2005.02804.x