Group 3 Innate Lymphoid Cells Protect the Host from the Uropathogenic Escherichia coli Infection in the Bladder
Innate lymphoid cells (ILCs) are crucial in orchestrating immunity and maintaining tissue homeostasis in various barrier tissues, but whether ILCs influence immune responses in the urinary tract remains poorly understood. Here, bladder‐resident ILCs are comprehensively explored and identified their...
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Published in | Advanced science Vol. 9; no. 6; pp. e2103303 - n/a |
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Main Authors | , , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Germany
John Wiley & Sons, Inc
01.02.2022
John Wiley and Sons Inc Wiley |
Subjects | |
Online Access | Get full text |
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Summary: | Innate lymphoid cells (ILCs) are crucial in orchestrating immunity and maintaining tissue homeostasis in various barrier tissues, but whether ILCs influence immune responses in the urinary tract remains poorly understood. Here, bladder‐resident ILCs are comprehensively explored and identified their unique phenotypic and developmental characteristics. Notably, bladder‐resident ILCs rapidly respond to uropathogenic Escherichia coli (UPEC) infection. It is found that ILC3 is necessary for early protection against UPEC infection in the bladder. Mechanistically, UPEC infection leads to interleukin (IL)‐1β production in the bladder via a MyD88‐dependent pathway, which promotes ILC3 activation. ILC3‐expressed IL‐17A further recruits neutrophils and controls UPEC infection in the bladder. Together, these results demonstrate a critical role for bladder ILCs in the host defense against UPEC infection.
Urinary tract infections by uropathogenic Escherichia coli (UPEC) are one of the most common bacterial infections worldwide. Innate lymphoid cells (ILCs), a novel population of immune cells, are found to be resident in the urinary tract. UPEC infection drives a rapid ILC3 response in the bladder. ILC3s further protect the host from UPEC infection through interleukin‐17‐mediated neutrophil recruitment. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 2198-3844 2198-3844 |
DOI: | 10.1002/advs.202103303 |