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Induction of proinflammatory mediators requires activation of the TRAF, NIK, IKK and NF-κB signal transduction pathway in astrocytes infected with Escherichia coli

 J. M. Kim  ;  Y.-K. Oh  ;  J. H. Lee  ;  D. Y. Im  ;  Y.-J. Kim  ;  J. Youn  ;  C.-H. Lee  ;  H. Son  ;  Y.-S. Lee  ;  J. Y. Park  ;  I.-H. Choi 
 Clinical and Experimental Immunology, Vol.140(3) : 450-460, 2005 
Journal Title
 Clinical and Experimental Immunology 
Issue Date
Escherichia coli is associated with inflammation in the brain. To investigate whether astrocytes are involved in E. coil-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-α, the CC chemokine MCP-1, TNF-α, and iNOS. E. coli infection 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 the E. 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 in E. coli-infected astrocytes via an NF-κB pathway, suggesting that these mediators may contribute to inflammation in the brain, including infiltration of inflammatory cells.
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1. College of Medicine (의과대학) > Dept. of Microbiology (미생물학교실) > 1. Journal Papers
Yonsei Authors
Choi, In Hong(최인홍) ORCID logo https://orcid.org/0000-0001-9851-0137
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