Open AccessThe type III secretion system is involved in the invasion and intracellular survival of Escherichia coli K1 in human brain microvascular endothelial cells
Author(s) -
Yao Yufeng,
Xie Yi,
Perace Donna,
Zhong Yi,
Lu Jie,
Tao Jing,
Guo Xiaokui,
Kim Kwang Sik
Publication year - 2009
Publication title -
fems microbiology letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.899
H-Index - 151
eISSN - 1574-6968
pISSN - 0378-1097
DOI - 10.1111/j.1574-6968.2009.01763.x
Subject(s) - escherichia coli , biology , mutant , microbiology and biotechnology , intracellular , secretion , bacteria , enterobacteriaceae , gene , pathogenesis , wild type , genetics , biochemistry , immunology
Type III secretion systems (T3SSs) have been documented in many Gram‐negative bacteria, including enterohemorrhagic Escherichia coli . We have previously shown the existence of a putative T3SS in meningitis‐causing E. coli K1 strains, referred to as E. coli type III secretion 2 (ETT2). The sequence of ETT2 in meningitis‐causing E. coli K1 strain EC10 (O7:K1) revealed that ETT2 comprises the epr, epa and eiv genes, but bears mutations, deletions and insertions. We constructed the EC10 mutants deleted of ETT2 or eivA gene, and their contributions to bacterial pathogenesis were evaluated in human brain microvascular endothelial cells (HBMECs). The deletion mutant of ETT2 exhibited defects in invasion and intracellular survival compared with the parental E. coli K1 strain EC10. The mutant deleted of eivA within ETT2 was also significantly defective in invasion and intracellular survival in HBMECs, and the defects of the eiv mutant were restored to the levels of the parent strain EC10 by transcomplementation. These findings suggest that ETT2 plays a role in the pathogenesis of E. coli K1 infection, including meningitis.