{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,24]],"date-time":"2026-10-24T13:22:37Z","timestamp":1792848157399,"version":"4.5.0"},"reference-count":72,"publisher":"MDPI AG","issue":"7","license":[{"start":{"date-parts":[[2026,7,20]],"date-time":"2026-07-20T00:00:00Z","timestamp":1784505600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Toxics"],"abstract":"<jats:p>As an emergent contaminant, 6-PPD quinone (6-PPDQ) causes toxic effects in organisms, including induction of immunosuppression. Thiamine pyrophosphate (TPP) serves as an important cofactor for some metabolisms. We aimed to examine the role of thiamine pyrophosphokinase TPK-1 in modulating 6-PPD-induced immunosuppression. Using Caenorhabditis elegans as the animal model, 6-PPDQ-exposure treatment was applied to nematodes from the L1 larval stage to adult day 3, and innate immune response was assessed by the expression of antimicrobial genes. In nematodes, 6-PPDQ (1\u201310 \u03bcg\/L) elevated TPP content, which was due to an increase in the expression of tpk-1, and RNAi of tpk-1 could block 6-PPDQ-induced immunosuppression. Meanwhile, RNAi of tpk-1 strengthened expressions of mitochondrial UPR (mt UPR) marker genes (hsp-6 and hsp-60) by activating three transcription factor (TF) genes (atfs-1, ubl-5, and dve-1) in 6-PPDQ-exposed nematodes. RNAi of mitochondrial UPR marker genes and three TF genes aggravated 6-PPDQ-induced immunosuppression. TPK-1 acted upstream of these three TF genes to modulate 6-PPDQ-induced immunosuppression. Moreover, RNAi of tpk-1 inhibited the expression of complex III\/IV subunit genes, and RNAi of these complex III\/IV subunit genes conferred resistance to 6-PPDQ-induced immunosuppression. Additionally, these complex III\/IV subunit genes functioned upstream of TF genes (atfs-1, ubl-5, and dve-1) to regulate 6-PPDQ-induced immunosuppression. Therefore, our data provide a novel basis for 6-PPDQ-induced immunosuppression mediated by activation of TPK-1 and the following mt UPR suppression.<\/jats:p>","DOI":"10.3390\/toxics14070630","type":"journal-article","created":{"date-parts":[[2026,7,20]],"date-time":"2026-07-20T12:00:17Z","timestamp":1784548817000},"page":"630","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Activation of Thiamine Pyrophosphokinase TPK-1 Contributes to 6-PPD Quinone-Induced Immunosuppression by Inhibiting Mitochondrial UPR in Caenorhabditis elegans"],"prefix":"10.3390","volume":"14","author":[{"given":"Zhe","family":"Wu","sequence":"first","affiliation":[{"name":"Key Laboratory of Environmental Medicine Engineering, Ministry of Education, School of Public Health, Southeast University, Nanjing 210009, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Guocheng","family":"Hu","sequence":"additional","affiliation":[{"name":"South China Institute of Environmental Sciences, Ministry of Ecology and Environment, Guangzhou 510655, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yunhui","family":"Li","sequence":"additional","affiliation":[{"name":"Key Laboratory of Environmental Medicine Engineering, Ministry of Education, School of Public Health, Southeast University, Nanjing 210009, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4656-7427","authenticated-orcid":false,"given":"Dayong","family":"Wang","sequence":"additional","affiliation":[{"name":"Medical School, Southeast University, Nanjing 210009, China"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2026,7,20]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"132265","DOI":"10.1016\/j.jhazmat.2023.132265","article-title":"Tire-rubber related pollutant 6-PPD quinone: A review of its transformation, environmental distribution, bioavailability, and toxicity","volume":"459","author":"Hua","year":"2023","journal-title":"J. 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