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IL-33 exacerbates acute kidney injury (CROSBI ID 180135)

Prilog u časopisu | izvorni znanstveni rad | međunarodna recenzija

Akcay, A., ... ; Pačić, Arijana ; Galešić Ljubanović, Danica ; ... ; Edelstein C.L. IL-33 exacerbates acute kidney injury // Journal of the American Society of Nephrology, 22 (2011), 11; 2057-2067. doi: 10.1681/ASN.2010091011

Podaci o odgovornosti

Akcay, A., ... ; Pačić, Arijana ; Galešić Ljubanović, Danica ; ... ; Edelstein C.L.

engleski

IL-33 exacerbates acute kidney injury

Inflammation contributes to the pathogenesis of acute kidney injury (AKI). IL-33 is a proinflammatory cytokine, but its role in AKI is unknown. Here we observed increased protein expression of full-length IL-33 in the kidney following induction of AKI with cisplatin. To determine whether IL-33 promotes injury, we administered soluble ST2 (sST2), a fusion protein that neutralizes IL-33 activity by acting as a decoy receptor. Compared with cisplatin-induced AKI in untreated mice, mice treated with sST2 had fewer CD4 T cells infiltrate the kidney, lower serum creatinine, and reduced acute tubular necrosis (ATN) and apoptosis. In contrast, administration of recombinant IL-33 (rIL-33) exacerbated cisplatin-induced AKI, measured by an increase in CD4 T cell infiltration, serum creatinine, ATN, and apoptosis ; this did not occur in CD4-deficient mice, suggesting that CD4 T cells mediate the injurious effect of IL-33. Wildtype mice that received cisplatin and rIL-33 also had higher levels of the proinflammatory chemokine CXCL1, which CD T cells produce, in the kidney compared with CD4-deficient mice. Mice deficient in the CXCL1 receptor also had lower serum creatinine, ATN, and apoptosis than wildtype mice following cisplatin-induced AKI. Taken together, IL-33 promotes AKI through CD4 T cell-mediated production of CXCL1. These data suggest that inhibiting IL-33 or CXCL1 may have therapeutic potential in AKI.

acute kidney injury; IL-33; cisplatin

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Podaci o izdanju

22 (11)

2011.

2057-2067

objavljeno

1046-6673

10.1681/ASN.2010091011

Povezanost rada

Temeljne medicinske znanosti

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