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Administration of ?-Galactosylceramide Improves Adenine-Induced Renal Injury.

ABSTRACT: Natural killer T (NKT) cells are a subset of lymphocytes that reacts to glycolipids presented by CD1d. Invariant NKT cells (iNKT) correspond to >90% of the total population of NKTs and reacts to ?-galactosylceramide (?GalCer). ?GalCer promotes a complex mixture of Th1 and Th2 cytokines, as interferon (IFN)-? and interleukin (IL)-4. NKT cells and IFN-? are known to participate in some models of renal diseases, but further studies are still necessary to elucidate their mechanisms. The aim of our study was to analyze the participation of iNKT cells in an experimental model of tubule-interstitial nephritis. We used 8-wk-old C57BL/6j, J?18KO and IFN-?KO mice. They were fed a 0.25% adenine diet for 10 d. Both adenine-fed wild-type (WT) and J?18KO mice exhibited renal dysfunction, but adenine-fed J?18KO mice presented higher expression of kidney injury molecule-1 (KIM-1), tumor necrosis factor (TNF)-? and type I collagen. To analyze the role of activated iNKT cells in our model, we administered ?GalCer in WT mice during adenine ingestion. After ?GalCer injection, we observed a significant reduction in serum creatinine, proinflammatory cytokines and renal fibrosis. However, this improvement in renal function was not observed in IFN-?KO mice after ?GalCer treatment and adenine feeding, illustrating that this cytokine plays a role in our model. Our findings may suggest that IFN-? production is one of the factors contributing to improved renal function after ?GalCer administration.

SUBMITTER: Aguiar CF

PROVIDER: S-EPMC4607613 | biostudies-literature | 2015 Jun

REPOSITORIES: biostudies-literature

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Administration of α-Galactosylceramide Improves Adenine-Induced Renal Injury.

Aguiar Cristhiane Favero CF Naffah-de-Souza Cristiane C Castoldi Angela A Corrêa-Costa Matheus M Braga Tárcio T TT Naka Érika L ÉL Amano Mariane T MT Abate Débora T R S DT Hiyane Meire I MI Cenedeze Marcos A MA Pacheco e Silva Filho Alvaro A Câmara Niels O S NO

Molecular medicine (Cambridge, Mass.) 20150618

Natural killer T (NKT) cells are a subset of lymphocytes that reacts to glycolipids presented by CD1d. Invariant NKT cells (iNKT) correspond to >90% of the total population of NKTs and reacts to α-galactosylceramide (αGalCer). αGalCer promotes a complex mixture of Th1 and Th2 cytokines, as interferon (IFN)-γ and interleukin (IL)-4. NKT cells and IFN-γ are known to participate in some models of renal diseases, but further studies are still necessary to elucidate their mechanisms. The aim of our s ...[more]

PMID: 26101952

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Project description:Background: Rhabdomyolysis (RM) is a clinical syndrome characterized by breakdown of skeletal muscle fibers and release of their contents into the circulation. Myoglobin-induced acute kidney injury (AKI) is one of the most severe complications of RM. Based on our previous research, exogenous biological renal support alleviates renal ischemia-reperfusion injury in elderly mice. This study aimed to determine whether exogenous biological renal support promotes renal recovery from RM-induced AKI and to preliminarily explore the mechanisms involved. Methods: A parabiosis animal model was established to investigate the effects of exogenous biological renal support on RM-induced AKI. Mice were divided into three groups: the control group (in which mice were injected with sterile saline), the RM group (in which mice were injected with 8 mL/kg glycerol), and the parabiosis + RM group (in which recipient mice were injected with glycerol 3 weeks after parabiosis model establishment). Blood samples and kidney tissue were collected for further processing 48 h after RM induction. Bioinformatics analysis was conducted via Gene Ontology analysis, Kyoto Encyclopedia of Genes and Genomes pathway analysis, functional enrichment analysis, and clustering analysis. Results: No mice died within 48 h after the procedure. Exogenous biological renal support attenuated the histological and functional deterioration in mice with RM-induced AKI. Bioinformatics analysis identified key pathways and proteins involved in this process. We further demonstrated that exogenous biological renal support ameliorated AKI through multiple mechanisms, including by suppressing the complement system; attenuating oxidative stress, inflammation, and cell death; and increasing proliferation. Conclusions: Exogenous biological renal support provided by parabiosis can improve renal function in RM-induced AKI by suppressing the complement system; decreasing oxidative stress, inflammation, and cell death; and promoting tubular cell proliferation. Our study provides basic research evidence for the use of bioartificial kidneys to treat RM-induced AKI.

Dataset Information

Administration of ?-Galactosylceramide Improves Adenine-Induced Renal Injury.

Publications

Administration of α-Galactosylceramide Improves Adenine-Induced Renal Injury.

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