UPEC hemolysin: More than just for making holes

Sheryl S. Justice; David A. Hunstad

doi:10.1016/j.chom.2012.01.001

UPEC hemolysin: More than just for making holes

Sheryl S. Justice, David A. Hunstad

Research output: Contribution to journal › Short survey › peer-review

13 Scopus citations

Abstract

During acute cystitis, uropathogenic Escherichia coli (UPEC) induce bladder epithelial cell exfoliation, which eliminates infected cells and promotes UPEC dissemination. Dhakal and Mulvey (2012) uncover the mechanism that induces this exfoliation and reintroduce the pore-forming toxin, hemolysin, as an effector that surprisingly targets multiple host pathways to facilitate infection.

Original language	English
Pages (from-to)	4-5
Number of pages	2
Journal	Cell Host and Microbe
Volume	11
Issue number	1
DOIs	https://doi.org/10.1016/j.chom.2012.01.001
State	Published - Jan 19 2012

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10.1016/j.chom.2012.01.001

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title = "UPEC hemolysin: More than just for making holes",

abstract = "During acute cystitis, uropathogenic Escherichia coli (UPEC) induce bladder epithelial cell exfoliation, which eliminates infected cells and promotes UPEC dissemination. Dhakal and Mulvey (2012) uncover the mechanism that induces this exfoliation and reintroduce the pore-forming toxin, hemolysin, as an effector that surprisingly targets multiple host pathways to facilitate infection.",

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AU - Hunstad, David A.

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N2 - During acute cystitis, uropathogenic Escherichia coli (UPEC) induce bladder epithelial cell exfoliation, which eliminates infected cells and promotes UPEC dissemination. Dhakal and Mulvey (2012) uncover the mechanism that induces this exfoliation and reintroduce the pore-forming toxin, hemolysin, as an effector that surprisingly targets multiple host pathways to facilitate infection.

AB - During acute cystitis, uropathogenic Escherichia coli (UPEC) induce bladder epithelial cell exfoliation, which eliminates infected cells and promotes UPEC dissemination. Dhakal and Mulvey (2012) uncover the mechanism that induces this exfoliation and reintroduce the pore-forming toxin, hemolysin, as an effector that surprisingly targets multiple host pathways to facilitate infection.

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