IL-17B protects against uropathogenic <i>E. coli</i> -induced kidney injury via macrophage infiltration modulation

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. IMPORTANCE: Urinary tract infections (UTIs) are a prevalent bacterial infectious disease that significantly affects women due to their recurrent nature and tissue damage. The increase of M1-type macrophages in infected kidneys is related to kidney injury. Investigating the mechanisms regulating macrophage infiltration could provide novel insights and strategies for treating UTIs. Previous studies have demonstrated the crucial role of IL-17A in modulating inflammation induced by UTIs, while the function of IL-17B remains poorly understood. Our research revealed that IL-17B deficiency enhanced macrophage infiltration and significantly increased mortality rates in mice during UTIs. Recombinant IL-17B treatment markedly alleviates renal damage caused by inflammation. These findings suggest that IL-17B could serve as a potential adjunctive therapeutic approach for severe UTIs, effectively controlling excessive inflammation-induced renal injury.