Journal
MICROBIAL PATHOGENESIS
Volume 45, Issue 3, Pages 181-191Publisher
ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.micpath.2008.05.006
Keywords
Enterobacter sakazakii; Outer membrane protein A; Endothelial cells; Protein kinase C-alpha; 1-Phosphatidylinositol 3-kinase; Microtubules
Categories
Funding
- PHS [AI40567]
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R29AI040567, R01AI040567] Funding Source: NIH RePORTER
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Enterobacter sakazakii (ES) causes neonatal meningitis and necrotizing enterocolitis with case-fatality rates among infected infants ranging from 40 to 80%. Very little is known about the mechanisms by which these organisms cause disease. Here, we demonstrate that ES invades human brain microvascular endothelial cells (HBMEC) with higher frequency when compared with epithelial cells and endothelial cells from different origins. The entry of ES into HBMEC requires the expression of outer membrane protein A (OmpA), as the OmpA-deletion mutant was sevenfold less invasive than the wild type ES and the bacterium does not multiply inside HBMEC. Anti-OmpA antibodies generated against the OmpA of Escherichia coli K1, which also recognize the OmpA of ES, did not prevent the invasion of ES in HBMEC. ES invasion depends on microtubule condensation in HBMEC and is independent of actin filament reorganization. Both PI3-kinase and PKC-alpha were activated during ES entry into HBMEC between 15 min and 30 min of infection. Concomitantly, overexpression of dominant negative forms of PI3-kinase and PKC-alpha significantly inhibited the invasion of ES into HBMEC. In summary, ES invasion of HBMEC is dependent on the expression of OmpA similar to that of E. coli K1; however, the epitopes involved in the interaction with HBMEC appears to be different. (C) 2008 Elsevier Ltd. All rights reserved.
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