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Antibacterial and Antifungal Agent, Triclosan (TCS) Alters Secretion of Interleukin beta and Interleukin 6 from Human Immune Cells
Author(s) -
Wilburn Wendy J.
Publication year - 2020
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.2020.34.s1.00517
Subject(s) - immune system , secretion , peripheral blood mononuclear cell , cytokine , interleukin , immunology , monocyte , chemistry , biology , pharmacology , endocrinology , biochemistry , in vitro
Triclosan (TCS) is an antimicrobial compound that is widely used in personal hygiene products such as mouthwash and toothpaste. TCS can be ingested or absorbed through the skin and has been found in human blood, breast milk, and urine. Interleukin (IL)‐6 and IL‐1 beta (IL‐1β) are important pro‐inflammatory cytokines produced by lymphocytes, monocytes, and other cells. Both regulate cell growth, tissue repair, and immune function, increased levels of each have been associated with a number of diseases including rheumatoid arthritis and certain cancers. TCS has been shown to inhibit the lytic function of human natural killer (NK) lymphocytes and to decrease expression of key cell surface proteins on NK cells. Here we examine whether TCS alters the secretion of IL‐1β and IL‐6 from human immune cell preparations. Human peripheral blood mononuclear cells (PBMCs) and monocyte‐depleted (MD)‐PBMCs were exposed to TCS at concentrations of 0–5 μM. Cytokine secretion was measured at 24 h, 48 h, and 6 days using enzyme‐linked immunosorbent assay (ELISA). In this study, both IL‐1β and IL‐6 secretion were altered at one or more concentration of TCS at one or more length of exposure. IL‐1β secretion was increased at 1, 2.5 or 5 μM TCS. Effects of 24 h exposure to 1, 2.5 and 5 μM TCS on IL‐1β secretion from PBMCs treated with selective MAPK pathway component inhibitors were also measured. These results indicate that TCS has the capacity to disrupt secretion of these two important pro‐inflammatory cytokines. Additionally the data show that TCS‐induced increases in IL‐β secretion were dependent on p38 MAPK. Support or Funding Information Supported by NIH grant U54CA163066.