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Updated: May 2, 2026

Establishment and Characterization of UTI and CAUTI in a Mouse Model
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IL-17B protects against uropathogenic E. coli-induced kidney injury via macrophage infiltration modulation

Changying Wang1,2, Min Liu1, Luyue Wang1

  • 1Institute of Immunology and Molecular Medicine, Jining Medical University, Jining, China.

Microbiology Spectrum
|May 1, 2026
PubMed

Urinary tract infections (UTIs) caused by uropathogenic Escherichia coli (UPEC) are prevalent among women. UPEC infection can lead to kidney injury, and currently, there are no effective methods to mitigate this damage. Previous studies have shown that macrophage infiltration is closely associated with kidney injury induced by UTIs. However, the mechanisms underlying macrophage recruitment to the kidneys remain unclear. In this study, IL-17B may play a critical role in protecting against UPEC-induced kidney injury by modulating macrophage infiltration and bacterial colonization. Compared with wild-type (WT) mice, IL-17B-/- mice exhibited significantly higher mortality and more M1-type macrophage infiltration, which was associated with renal injury. rIL-17B treatment significantly reduced macrophage infiltration in the kidneys of CFT073-infected mice. Additionally, analysis of chemokines indicated that IL-17B is a key regulator of macrophage recruitment by influencing the expression of CCL2, CCL3, and CCL7. Overall, IL-17B can serve as a crucial cytokine for treating urinary tract infections and mitigating kidney damage.

Keywords:
IL-17Bchemokineskidney injurymacrophagesuropathogenic Escherichia coli

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