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TBT has been detected in human blood at concentrations up to 260 nM, DBT up to 0.3 \u00b5M, and PCP between 0.15 and 5 \u00b5M. Tumor necrosis factor-alpha (TNF-\u03b1) is a pro-inflammatory cytokine produced by immune cells in response to pathogen- or damage-associated molecular patterns (PAMPs\/DAMPs) via Toll-like receptors (TLRs). Dysregulated TNF-\u03b1 production contributes to chronic inflammatory pathology. Previous studies have shown that TBT, DBT, and PCP increase pro-inflammatory cytokine production by immune cells and that these increases depend on mitogen-activated protein kinases (MAPKs), which are downstream components of TLR activation. The current study indicates that TLR4 plays a role in TBT-, DBT-, and PCP-induced production of TNF-\u03b1. Additionally, TBT-induced TNF-\u03b1 production was, at least in part, dependent on TLR2, DBT-induced TNF-\u03b1 production on TLR1\/2 and PCP-induced TNF-\u03b1 production on TLR3 and TLR8. Blocking the initial component of TLR1\/2, TLR2, TLR4, and TLR8 signaling, MyD88, led to very significant blockade of TBT- and PCP-induced TNF-\u03b1 production. These findings provide additional understanding as to how compounds that are persistent pollutants activate production of a crucial regulator of inflammation, TNF-\u03b1, potentially contributing to chronic inflammation and its associated diseases.<\/jats:p>","DOI":"10.1007\/s00204-026-04522-9","type":"journal-article","created":{"date-parts":[[2026,8,25]],"date-time":"2026-08-25T01:59:33Z","timestamp":1787623173000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["The role of toll-like receptors in tributyltin-, dibutyltin-, and pentachlorophenol-induced stimulation of tumor necrosis factor-alpha (TNF\u03b1) production in human immune cells"],"prefix":"10.1007","author":[{"given":"Latoya M.","family":"Daniel","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Aleshia","family":"Seaton-Terry","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ellie","family":"Bray","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Meaghan","family":"Lewis","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zinia","family":"Hunter","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sophia","family":"Fisher","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Brian","family":"Townsend","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1511-9181","authenticated-orcid":false,"given":"Margaret M.","family":"Whalen","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2026,8,25]]},"reference":[{"issue":"8","key":"4522_CR1","doi-asserted-by":"publisher","first-page":"2244","DOI":"10.3390\/ijms19082244","volume":"19","author":"SO Adegbola","year":"2018","unstructured":"Adegbola SO, Sahnan K, Warusavitarne J, Hart A, Tozer P (2018) Anti-TNF therapy in Crohn\u2019s disease. 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