antibody-directed glucocorticoid targeting to cd163 in m2-type macrophages attenuates fructose-induced liver inflammatory changes
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2017
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Abstract
Increased consumption of high-caloric carbohydrates contributes substantially to endemic non-alcoholic fatty liver disease in humans, covering a histological spectrum from fatty liver to steatohepatitis. Hypercaloric intake and lipogenetic effects of fructose and endotoxin-driven activation of liver macrophages are suggested to be essential to disease progression. In the present study, we show that a low dose of an anti-CD163-IgG-dexamethasone conjugate targeting the hemoglobin scavenger receptor CD163 in Kupffer cells and other M2-type macrophages has a profound effect on liver inflammatory changes in rats on a high-fructose diet. The diet induced severe non-alcoholic steatohepatitis (NASH)-like changes within a few weeks but the antibody-drug conjugate strongly reduced inflammation, hepatocyte ballooning, fibrosis, and glycogen deposition. Non-conjugated dexamethasone or dexamethasone conjugated to a control IgG did not have this effect but instead exacerbated liver lipid accumulation. The low-dose anti-CD163-IgG-dexamethasone conjugate displayed no apparent systemic side effects. In conclusion, macrophage targeting by antibody-directed anti-inflammatory low-dose glucocorticoid therapy seems to be a promising approach for safe treatment of fructose-induced liver inflammation.
| Reference Key |
svendsen2017molecularantibody-directed
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|---|---|
| Authors | ;Pia Svendsen;Jonas H. Graversen;Anders Etzerodt;Henrik Hager;Rasmus Røge;Henning Grønbæk;Erik I. Christensen;Holger J. Møller;Hendrik Vilstrup;Søren K. Moestrup |
| Journal | international journal of zoology |
| Year | 2017 |
| DOI |
10.1016/j.omtm.2016.11.004
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| URL | |
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