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Cell Host Microbe. 2013 Dec 11;14(6):664-74. doi: 10.1016/j.chom.2013.11.004.

Natural killer cell-mediated host defense against uropathogenic E. coli is counteracted by bacterial hemolysinA-dependent killing of NK cells.

Author information

1
The Lautenberg Center of General and Tumor Immunology, The Hebrew University Hadassah Medical School, IMRIC, Jerusalem 91120, Israel; Internal Medicine Department, Hadassah Medical Center, Jerusalem 91120, Israel.
2
The Institute of Dental Sciences, Hebrew University-Hadassah School of Dental Medicine, Jerusalem 91120, Israel.
3
Urology Department, Hadassah Medical Center, Jerusalem 91120, Israel.
4
The Lautenberg Center of General and Tumor Immunology, The Hebrew University Hadassah Medical School, IMRIC, Jerusalem 91120, Israel.
5
The Lautenberg Center of General and Tumor Immunology, The Hebrew University Hadassah Medical School, IMRIC, Jerusalem 91120, Israel; The Institute of Dental Sciences, Hebrew University-Hadassah School of Dental Medicine, Jerusalem 91120, Israel.
6
Internal Medicine Department, Hadassah Medical Center, Jerusalem 91120, Israel.
7
Department of Developmental Biology and Cancer Research, The Hebrew University Hadassah Medical School, IMRIC, Jerusalem 91120, Israel.
8
The Institute of Dental Sciences, Hebrew University-Hadassah School of Dental Medicine, Jerusalem 91120, Israel. Electronic address: giladba@ekmd.huji.ac.il.
9
The Lautenberg Center of General and Tumor Immunology, The Hebrew University Hadassah Medical School, IMRIC, Jerusalem 91120, Israel. Electronic address: oferm@ekmd.huji.ac.il.

Abstract

Uropathogenic Escherichia coli (UPEC) are a common cause of urinary tract infections (UTIs) in humans. While the importance of natural killer (NK) cells in innate immune protection against tumors and viral infections is well documented, their role in defense against bacterial infections is still emerging, and their involvement in UPEC-mediated UTI is practically unknown. Using a systematic mutagenesis approach, we found that UPEC adheres to NK cells primarily via its type I fimbriae and employs its hemolysinA toxin to kill NK cells. In the absence of hemolysinA, NK cells directly respond to the bacteria and secrete the cytokine TNF-α, which results in decreased bacterial numbers in vitro and reduction of bacterial burden in the infected bladders. Thus, NK cells control UPEC via TNF-α production, which UPEC counteracts by hemolysinA-mediated killing of NK cells, representing a previously unrecognized host defense and microbial counterattack mechanism in the context of UTI.

PMID:
24331464
PMCID:
PMC3868942
DOI:
10.1016/j.chom.2013.11.004
[Indexed for MEDLINE]
Free PMC Article

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