Interleukin-15-mediated inflammation promotes non-alcoholic fatty liver disease. Cytokine 2016 Jun;82:102-11
Date
02/13/2016Pubmed ID
26868085DOI
10.1016/j.cyto.2016.01.020Scopus ID
2-s2.0-84956921610 (requires institutional sign-in at Scopus site) 49 CitationsAbstract
Interleukin-15 (IL-15) is essential for the homeostasis of lymphoid cells particularly memory CD8(+) T cells and NK cells. These cells are abundant in the liver, and are implicated in obesity-associated pathogenic processes. Here we characterized obesity-associated metabolic and cellular changes in the liver of mice lacking IL-15 or IL-15Rα. High fat diet-induced accumulation of lipids was diminished in the livers of mice deficient for IL-15 or IL-15Rα. Expression of enzymes involved in the transport of lipids in the liver showed modest differences. More strikingly, the liver tissues of IL15-KO and IL15Rα-KO mice showed decreased expression of chemokines CCl2, CCL5 and CXCL10 and reduced infiltration of mononuclear cells. In vitro, IL-15 stimulation induced chemokine gene expression in wildtype hepatocytes, but not in IL15Rα-deficient hepatocytes. Our results show that IL-15 is implicated in the high fat diet-induced lipid accumulation and inflammation in the liver, leading to fatty liver disease.
Author List
Cepero-Donates Y, Lacraz G, Ghobadi F, Rakotoarivelo V, Orkhis S, Mayhue M, Chen YG, Rola-Pleszczynski M, Menendez A, Ilangumaran S, Ramanathan SAuthor
Yi-Guang Chen PhD Professor in the Pediatrics department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
AnimalsCD8-Positive T-Lymphocytes
Chemokines
Dietary Fats
Hepatocytes
Immunologic Memory
Inflammation
Interleukin-15
Killer Cells, Natural
Mice
Mice, Knockout
Non-alcoholic Fatty Liver Disease
Receptors, Interleukin-15
