@Article{ecn.2006.0042,
AUTHOR = {Emmanouil Galanakis, Francescopaolo Di Cello, Maneesh Paul-Satyaseela, Kwang Sik Kim},
TITLE = {<i>Escherichia coli</i> K1 induces IL-8 expression in human brain microvascular endothelial cells},
JOURNAL = {European Cytokine Network},
VOLUME = {17},
YEAR = {2006},
NUMBER = {4},
PAGES = {260--265},
URL = {http://www.techscience.com/ECN/v17n4/66137},
ISSN = {1952-4005},
ABSTRACT = {Microbial penetration of the blood-brain barrier (BBB) into the central nervous system is essential
for the development of meningitis. Considerable progress has been achieved in understanding the pathophysiology
of meningitis, however, relatively little is known about the early inflammatory events occurring at the time of
bacterial crossing of the BBB. We investigated, using real-time quantitative PCR, the expression of the neutrophil
chemoattractants alpha-chemokines CXCL1 (Groa) and CXCL8 (IL-8), and of the monocyte chemoattractant
beta-chemokine CCL2 (MCP-1) by human brain microvascular endothelial cells (HBMEC) in response to the
meningitis-causing <i>E. coli</i> K1 strain RS218 or its isogenic mutants lacking the ability to bind to and invade
HBMEC. A nonpathogenic, laboratory <i>E. coli</i> strain HB101 was used as a negative control. CXCL8 was shown
to be significantly expressed in HBMEC 4 hours after infection with <i>E. coli</i> K1, while no significant alterations
were noted for CXCL1 and CCL2 expression. This upregulation of CXCL8 was induced by <i>E. coli</i> K1 strain
RS218 and its derivatives lacking the ability to bind and invade HBMEC, but was not induced by the laboratory
strain HB101. In contrast, no upregulation of CXCL8 was observed in human umbilical vein endothelial cells
(HUVEC) after stimulation with <i>E. coli</i> RS218. These findings indicate that the CXCL8 expression is the result
of the specific response of HBMEC to meningitis-causing <i>E. coli</i> K1.},
DOI = {10.1684/ecn.2006.0042}
}