Natural Killer Cell-Mediated Host Defense against Uropathogenic E. coli Is Counteracted by Bacterial HemolysinA-Dependent Killing of NK Cells
| Autor: | Ronit Naor, Dror Mevorach, Omer Fleissig, Rachel Yamin, Ofer Mandelboim, Ariella Glasner, Jawad Abed, Chamutal Gur, Zvi Granot, Shunit Coppenhagen-Glazer, Yotam Bar-On, Gilad Bachrach, Jonatan Enk, Shilo Rosenberg |
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| Rok vydání: | 2013 |
| Předmět: |
Cancer Research
Cell Survival Virulence Factors medicine.medical_treatment Context (language use) Biology medicine.disease_cause urologic and male genital diseases Microbiology Article Natural killer cell Gene Knockout Techniques Hemolysin Proteins Mice 03 medical and health sciences Virology Immunology and Microbiology(all) medicine Animals Humans Uropathogenic Escherichia coli Secretion Escherichia coli Molecular Biology Cells Cultured 030304 developmental biology 0303 health sciences Innate immune system Tumor Necrosis Factor-alpha 030306 microbiology Escherichia coli Proteins bacterial infections and mycoses Bacterial Load female genital diseases and pregnancy complications 3. Good health Killer Cells Natural Mice Inbred C57BL Mutagenesis Insertional Cytokine medicine.anatomical_structure Host-Pathogen Interactions Immunology DNA Transposable Elements Interleukin 12 Parasitology Tumor necrosis factor alpha |
| Zdroj: | Cell Host & Microbe |
| ISSN: | 1931-3128 |
| DOI: | 10.1016/j.chom.2013.11.004 |
| Popis: | SummaryUropathogenic 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. |
| Databáze: | OpenAIRE |
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