IL-36 expression plays a potential role in acute kidney injury through down-regulation of inflammatory response

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Pathophysiology of Cell Injury Journal  Volume 5, Issue 1, pages 16-26
Received December 01, 2015; accepted May 12, 2016; published June 11, 2016

Heather B. Hatcher¹, Yukio Tsung², Shao-Ling Qin¹’², Chris A Clarkson, Mao Zhao¹*



The inflammatory response following acute kidney injury (AKI) contributed in many pathological pathways that involved in renal failure. IL-36 is member of the IL-1 family of cytokines and recently found it expressed in blood and correlated to the tissue injury. However, the role of IL-36 role in AKI remains unclear. This study investigated a potential role for IL-36 in down-regulation of the inflammatory response following AKI. Acute ischemia and reperfusion operation were performed sham on male C57BL/6J and IL-36-/- mice. The inflammatory response markly decreased with mice loss the IL-36, rsulted in suppression of (IL-6, IL-1ß, TN-alfa). The infiltration of peritubular neutrophils was attenuated in IL-36-/- mice with reduced the plasma levels of blood urea and serum creatinin, further data demonstrated that less apoptosis in IL-36-/- under AKI. This study discussed the possibility of protective role with antagonised the effects of IL-36 in AKI and more investigation needs.

Keywords: IL-36; Acute kidney injury; Neutrophils

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