Premium
Effects of tributyltin exposures on secretion of interleukin 1 beta from human immune cells (1012.1)
Author(s) -
Brown Shyretha,
Whalen Margaret
Publication year - 2014
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.28.1_supplement.1012.1
Subject(s) - tributyltin , immune system , secretion , peripheral blood mononuclear cell , monocyte , interleukin , cytokine , chemistry , biology , immunology , endocrinology , biochemistry , in vitro , organic chemistry
Tributyltin (TBT) is an organotin compound used as a biocide in a variety of industrial applications such as wood preservation and as an antifungal. It has been found in human blood samples. Interleukin 1 beta (IL‐1β) is produced by monocytes and macrophages and promotes cell growth, tissue repair, and regulates immune response. IL‐1β appears to increase the invasiveness of certain tumors. The aim of the current study is to determine if exposures to TBT modify secretion of IL‐1β from increasingly reconstituted preparations of human immune cells. TBT concentrations of 25 to 200 nM at 24h, 48h, or 6 days were examined in highly enriched human NK cells, monocyte‐depleted human peripheral blood mononuclear cells (PBMCs), PBMCs, granulocytes, and a combination of PBMCs and granulocytes. IL‐1β was measured using an enzyme‐linked immunosorbent assay (ELISA). Results show TBT alters IL‐1β secretion from all cells preparations. 200 nM concentrations of TBT blocked the secretion of IL‐1β, while lower concentrations of TBT elevated secretion of IL‐1β. Concentrations and lengths of exposure to TBT that caused statistically significant increases in IL‐1β secretion from human immune cells varied from one donor to the next. The data indicates that TBT‐induced alterations of IL‐1β secretion from immune cells may be a significant consequence of TBT exposures that may potentially affect immune competence and cancer invasiveness. Grant Funding Source : Supported by NIH grant 5U54CA163066‐02