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25 (OH) D3 treatment improves inflammatory pathway on monocytes lineage (U937) in uremic environment
Author(s) -
Oliveira Brito Rodrigo Barbosa,
Rebello Jacqueline Ferritto,
Santos Oliveira Willian Rubens,
Grabulosa Caren Cristina,
Matos Yves Siva Teles,
Malta Camila Soares,
Dellê Humberto,
Dalboni Maria Aparecida
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.695.4
Subject(s) - calcitriol receptor , cathelicidin , cd14 , uremia , inflammation , vitamin d and neurology , medicine , uremic toxins , endocrinology , monocyte , flow cytometry , oxidative stress , vitamin d deficiency , kidney disease , receptor , immunology , innate immune system
The chronic kidney disease (CKD) is characterized by an inflammatory state caused by the presence of uremic toxins in plasma of patients. This inflammatory condition is associated with a higher risk for cardiovascular diseases and infections. In CKD there is a deficiency of vitamin 25 (OH) D, which has immunomodulatory properties, and that supplementation of the same can decrease inflammation present in uremia. The aim of this study was to evaluate the effect of 25 (OH) D of inflammatory pathways such as toll like receptor 4 (TRL4), oxidative stress (ROS) and expression of vitamin D receptor (VDR), 1‐α hydroxylase, 24‐hydroxylase and inflammatory mediators in monocytes in uremic environment. The monocyte U937 cell line were treated with or without 25 (OH) D 50ng/ml for 24 hours and then they were incubated with 50% serum of healthy patients or uremic patient sera Durantes 24 hours at 37 °C and 5 CO2. The monocytes were characterized by expression of CD14 + cells. The TRL4, VDR, CYP24, Cyp27 and ROS was evaluated by flow cytometry. It was performed in the cell culture supernatant ELISA for IL‐6, TNF‐α, IL‐10, MCP‐1 and cathelicidin. We observed a high expression of TRL‐4, IL‐6, TNF‐α, IL‐10 cathelicidin and MCP‐1 in monocytes incubated with uremic serum, when compared incubated with healthy serum. Pretreatment with 25 (OH) D were able to reduce the expression TRL4, cathelicidin‐1 and MCP opposite uremic environment. There was no difference in the expression of VDR and CYP27 and CYP24 enzymes. We conclude that the uremic environment induces inflammation by increasing TRL4 and inflammatory mediators and the vitamin D treatment indicates an improvement in the inflammatory parameters and may result in reduced inflammation in uremic environment. Support or Funding Information FAPESP 2014/14192‐1