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IL-36 alpha Regulates Tubulointerstitial Inflammation in the Mouse Kidney

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Title: IL-36 alpha Regulates Tubulointerstitial Inflammation in the Mouse Kidney
Authors: Ichii, Osamu Browse this author →KAKEN DB
Kimura, Junpei Browse this author
Okamura, Tadashi Browse this author
Horino, Taro Browse this author
Nakamura, Teppei Browse this author
Sasaki, Hayato Browse this author
Elewa, Yaser Hosny Ali Browse this author →ORCID
Kon, Yasuhiro Browse this author →KAKEN DB
Keywords: inflammation
distal tubule
IL-36 alpha
tubulointerstitial lesion
unilateral ureter obstruction
folic acid
Issue Date: 23-Oct-2017
Publisher: Frontiers Media
Journal Title: Frontiers in immunology
Volume: 8
Start Page: 1346
Publisher DOI: 10.3389/fimmu.2017.01346
Abstract: IL-36 alpha, a member of the IL-1 family, is a crucial mediator of inflammatory responses. We previously found that IL-36 alpha was overexpressed in injured distal tubules (DTs); however, its pathological function remains unclear. Herein, unilateral ureter obstruction (UUO) or folic acid (FA) injection was performed in mouse kidneys to assess the role of IL-36 alpha in kidney injury. IL-36 alpha mRNA and protein expression significantly increased in the kidneys within 24 h after UUO. IL-36 alpha localized to dilated DTs. IL-36 alpha expression significantly correlated with the progression of tubulointerstitial cell infiltration and tubular epithelium cell death in UUO kidneys and with renal dysfunction in FA-induced acute kidney injury mice. At 24 h after UUO, IL-36 alpha(+) DT epithelial cells showed loose intercellular digitations. IL-1RL2, an IL-36 alpha receptor protein, localized to podocytes, proximal tubules, and DTs in the healthy kidney. IL-1RL2 was expressed in interstitial cells and platelets or extended primary cilia of DT epithelial cells in UUO kidneys. IL-36 alpha stimulation promoted the production of IL-6 and Prss35, an inflammatory cytokine and collagen remodeling-associated enzyme, respectively, in cultured NIH3T3 fibroblasts. UUO-treated IL-36 alpha-knockout (KO) mice showed milder kidney injury features than wild-type (WT) mice did. In UUO kidneys from IL-36 alpha-KO mice, the expression of genes associated with inflammatory response and sensory perception was significantly different from that in WT mice. Altogether, our data indicate an association between intrarenal IL-36 alpha overexpression and the progression of tubulointerstitial inflammations and morpho-functional alterations of DT epithelial cells. IL-36 alpha may be a novel kidney injury marker useful for evaluating DT damages.
Rights: © 2017 Ichii, Kimura, Okamura, Horino, Nakamura, Sasaki, Elewa and Kon
https://creativecommons.org/licenses/by/4.0/
Type: article
URI: http://hdl.handle.net/2115/70804
Appears in Collections:獣医学院・獣医学研究院 (Graduate School of Veterinary Medicine / Faculty of Veterinary Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 市居 修

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