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Signaling Pathways Involved in Tributyltin‐Induced Increases in Interleukin 6 Production by Lymphocytes
Author(s) -
Hamza Nafisa,
Brown Shyretha,
Whalen Margaret
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.615.1
Subject(s) - tributyltin , microbiology and biotechnology , mapk/erk pathway , p38 mitogen activated protein kinases , tumor necrosis factor alpha , chemistry , cytokine , stimulation , interleukin , signal transduction , biology , immunology , endocrinology , environmental chemistry
Tributyltin (TBT) is a toxic compound that has industrial uses, such as slime control on masonry, wood preservation, and disinfection of circulating industrial cooling water and is most frequently used in antifouling paints on the hulls of ships. As a result of TBT's lipophilic character, it absorbs readily into organisms and contaminates the environment and is found in human blood in concentrations as high as 261 nM. TBT decreases the lytic function and secretion of interferon gamma (IFNγ), tumor necrosis factor alpha and interleukin 1 beta (IL‐1β) from human lymphocytes. IL‐6 is a cytokine which regulates the function of many cells including tumor cells. Recent studies in our lab have shown that TBT alters production of IL‐6 by lymphocytes. The current study aims to determine whether TBT utilizes MAPK signaling pathways (ERK 1/2, p38) to cause alterations in IL‐6 production. TBT‐induced production of IL‐6 in human lymphocytes was measured in the presence and absence of ERK1/2 pathway (PD98059) and p38 (SB202190). Results indicated that the stimulation of IL‐6 production by TBT decreased in the presence of each of the MAPK pathway inhibitors. These data suggest that TBT may be causing increased IL‐6 production by activating ERK1/2 and p38 MAPKs. Support or Funding Information Supported by NIH grant 5U54CA163066