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Nucleoside-diphosphate kinase of uropathogenic Escherichia coli inhibits caspase-1-dependent pyroptosis facilitating urinary tract infection.

التفاصيل البيبلوغرافية
العنوان: Nucleoside-diphosphate kinase of uropathogenic Escherichia coli inhibits caspase-1-dependent pyroptosis facilitating urinary tract infection.
المؤلفون: Li X; TEDA Institute of Biological Sciences and Biotechnology, Nankai University, Tianjin 300457, P.R. China; The Key Laboratory of Molecular Microbiology and Technology, TEDA Institute of Biological Sciences and Biotechnology, Nankai University, Ministry of Education, Tianjin 300457, P.R. China., Zhou J; TEDA Institute of Biological Sciences and Biotechnology, Nankai University, Tianjin 300457, P.R. China; The Key Laboratory of Molecular Microbiology and Technology, TEDA Institute of Biological Sciences and Biotechnology, Nankai University, Ministry of Education, Tianjin 300457, P.R. China., Liu X; TEDA Institute of Biological Sciences and Biotechnology, Nankai University, Tianjin 300457, P.R. China; The Key Laboratory of Molecular Microbiology and Technology, TEDA Institute of Biological Sciences and Biotechnology, Nankai University, Ministry of Education, Tianjin 300457, P.R. China., Jin C; TEDA Institute of Biological Sciences and Biotechnology, Nankai University, Tianjin 300457, P.R. China; The Key Laboratory of Molecular Microbiology and Technology, TEDA Institute of Biological Sciences and Biotechnology, Nankai University, Ministry of Education, Tianjin 300457, P.R. China., Liu L; TEDA Institute of Biological Sciences and Biotechnology, Nankai University, Tianjin 300457, P.R. China; The Key Laboratory of Molecular Microbiology and Technology, TEDA Institute of Biological Sciences and Biotechnology, Nankai University, Ministry of Education, Tianjin 300457, P.R. China., Sun H; TEDA Institute of Biological Sciences and Biotechnology, Nankai University, Tianjin 300457, P.R. China; The Key Laboratory of Molecular Microbiology and Technology, TEDA Institute of Biological Sciences and Biotechnology, Nankai University, Ministry of Education, Tianjin 300457, P.R. China., Wang Q; TEDA Institute of Biological Sciences and Biotechnology, Nankai University, Tianjin 300457, P.R. China; The Key Laboratory of Molecular Microbiology and Technology, TEDA Institute of Biological Sciences and Biotechnology, Nankai University, Ministry of Education, Tianjin 300457, P.R. China., Wang Q; TEDA Institute of Biological Sciences and Biotechnology, Nankai University, Tianjin 300457, P.R. China; The Key Laboratory of Molecular Microbiology and Technology, TEDA Institute of Biological Sciences and Biotechnology, Nankai University, Ministry of Education, Tianjin 300457, P.R. China., Liu R; TEDA Institute of Biological Sciences and Biotechnology, Nankai University, Tianjin 300457, P.R. China; The Key Laboratory of Molecular Microbiology and Technology, TEDA Institute of Biological Sciences and Biotechnology, Nankai University, Ministry of Education, Tianjin 300457, P.R. China., Zheng X; TEDA Institute of Biological Sciences and Biotechnology, Nankai University, Tianjin 300457, P.R. China; The Key Laboratory of Molecular Microbiology and Technology, TEDA Institute of Biological Sciences and Biotechnology, Nankai University, Ministry of Education, Tianjin 300457, P.R. China., Liu Y; TEDA Institute of Biological Sciences and Biotechnology, Nankai University, Tianjin 300457, P.R. China; The Key Laboratory of Molecular Microbiology and Technology, TEDA Institute of Biological Sciences and Biotechnology, Nankai University, Ministry of Education, Tianjin 300457, P.R. China. Electronic address: liuyutao623@nankai.edu.cn., Pang Y; TEDA Institute of Biological Sciences and Biotechnology, Nankai University, Tianjin 300457, P.R. China; The Key Laboratory of Molecular Microbiology and Technology, TEDA Institute of Biological Sciences and Biotechnology, Nankai University, Ministry of Education, Tianjin 300457, P.R. China. Electronic address: pangyu@nankai.edu.cn.
المصدر: Cell reports [Cell Rep] 2024 Apr 23; Vol. 43 (4), pp. 114051. Date of Electronic Publication: 2024 Apr 01.
نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: Cell Press Country of Publication: United States NLM ID: 101573691 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 2211-1247 (Electronic) NLM ISO Abbreviation: Cell Rep Subsets: MEDLINE
أسماء مطبوعة: Original Publication: [Cambridge, MA] : Cell Press, c 2012-
مواضيع طبية MeSH: Uropathogenic Escherichia coli*/pathogenicity , Urinary Tract Infections*/microbiology , Urinary Tract Infections*/pathology , Pyroptosis* , Caspase 1*/metabolism , Nucleoside-Diphosphate Kinase*/metabolism , Nucleoside-Diphosphate Kinase*/genetics , Escherichia coli Infections*/microbiology , Escherichia coli Infections*/metabolism , Escherichia coli Infections*/pathology, Animals ; Mice ; Reactive Oxygen Species/metabolism ; Mice, Inbred C57BL ; Humans ; Female ; Urinary Bladder/microbiology ; Urinary Bladder/pathology ; Epithelial Cells/microbiology ; Epithelial Cells/metabolism ; Escherichia coli Proteins/metabolism ; Escherichia coli Proteins/genetics ; Signal Transduction
مستخلص: Uropathogenic Escherichia coli (UPEC) is the most common causative agent of urinary tract infection (UTI). UPEC invades bladder epithelial cells (BECs) via fusiform vesicles, escapes into the cytosol, and establishes biofilm-like intracellular bacterial communities (IBCs). Nucleoside-diphosphate kinase (NDK) is secreted by pathogenic bacteria to enhance virulence. However, whether NDK is involved in UPEC pathogenesis remains unclear. Here, we find that the lack of ndk impairs the colonization of UPEC CFT073 in mouse bladders and kidneys owing to the impaired ability of UPEC to form IBCs. Furthermore, we demonstrate that NDK inhibits caspase-1-dependent pyroptosis by consuming extracellular ATP, preventing superficial BEC exfoliation, and promoting IBC formation. UPEC utilizes the reactive oxygen species (ROS) sensor OxyR to indirectly activate the regulator integration host factor, which then directly activates ndk expression in response to intracellular ROS. Here, we reveal a signaling transduction pathway that UPEC employs to inhibit superficial BEC exfoliation, thus facilitating acute UTI.
Competing Interests: Declaration of interests The authors declare no competing interests.
(Copyright © 2024 The Author(s). Published by Elsevier Inc. All rights reserved.)
فهرسة مساهمة: Keywords: BEC exfoliation; CP: Cell biology; CP: Microbiology; NDK; UPEC; caspase-1 activation; pyroptosis
المشرفين على المادة: EC 3.4.22.36 (Caspase 1)
EC 2.7.4.6 (Nucleoside-Diphosphate Kinase)
0 (Reactive Oxygen Species)
0 (Escherichia coli Proteins)
تواريخ الأحداث: Date Created: 20240402 Date Completed: 20240426 Latest Revision: 20240510
رمز التحديث: 20240511
DOI: 10.1016/j.celrep.2024.114051
PMID: 38564334
قاعدة البيانات: MEDLINE
الوصف
تدمد:2211-1247
DOI:10.1016/j.celrep.2024.114051