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. 2009 Dec 14;120(1):331–342. doi: 10.1172/JCI38702

Figure 2. Activation of the IL-23/IL-17A/IL-17R pathway following kidney IRI increases kidney expression of proinflammatory cytokines and chemokines that mediate neutrophil recruitment.

Figure 2

(A and B) Blocking CXCR2 attenuated kidney IRI inflammation. (A) Plasma creatinine levels in WT mice that received anti-CXCR2 goat serum or goat serum control 18 hours and 1 hour prior to sham or IRI. n = 4–6; **P < 0.01. (B) Kidney morphology evaluated by H&E staining. Arrowheads indicate tubular injury. Scale bar: 10 μm. (C and D) Kidney mRNA expression level (C) of IL-23/IL-17 downstream cytokines (Tfna and Il6) and neutrophil chemoattractant chemokines (Cxcl1 and Cxcl2) was measured by real-time PCR at different time points following kidney reperfusion (2, 4, 6, and 24 hours; n = 2–5. *P < 0.05; ***P < 0.001 compared with sham) and (D) in WT, p40–/–, p19–/–, Il17a–/–, and Il17r–/– mice after 6 hours of kidney reperfusion (n = 2–8; *P < 0.05 compared with KO mice). Values are mean ± SEM.