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Interleukin 1β and interleukin 6 production in human immune cells is stimulated by the antibacterial compound Triclosan

  • Immunotoxicology
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Abstract

Triclosan (TCS) is an antimicrobial compound widely used in personal hygiene products such as mouthwash and toothpaste; and has been found in human blood, breast milk, and urine. Interleukin (IL)-6 and IL-1 beta (IL-1β) are pro-inflammatory cytokines regulating cell growth, tissue repair, and immune function; increased levels of each have been associated with many diseases, including cancer. Previous studies showed that TCS at concentrations between 0.05 and 5 µM consistently increased the secretion of IL-1β and IL-6 from human immune cells within 24 h of exposure. The current study demonstrates that this increase in secretion was not due simply to release of existing stores but was due to an increase in cellular production/levels (both secreted and intracellular levels) of each of these cytokines. Production of IL-1β and IL-6 was increased by exposure to one or more concentration of TCS at each length of exposure (10 min, 30 min, 6 h, and 24 h). TCS-induced stimulation of cytokine production was shown to be dependent on the mitogen-activated protein kinase (MAPK) p44/42 (ERK 1/2). It was also shown that these TCS-induced increases in IL-1β and IL6 production were accompanied by increased mRNA for IL-1β and IL-6. The ability of TCS to increase production indicates that rather than activating a self-limiting process of depleting cells of already existing stores of IL-1β or IL-6, TCS can stimulate a process that has the capacity to provide sustained production of these cytokines and thus may lead to chronic inflammation and its pathological consequences.

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Acknowledgements

Supported by Grant U54CA163066 and 5T34GM007663 from the National Institutes of Health.

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Correspondence to Margaret M. Whalen.

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Wilburn, W.J., Gabure, S. & Whalen, M.M. Interleukin 1β and interleukin 6 production in human immune cells is stimulated by the antibacterial compound Triclosan. Arch Toxicol 98, 883–895 (2024). https://doi.org/10.1007/s00204-023-03654-6

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