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. 2022 Jan 13;12:656. doi: 10.1038/s41598-021-04562-4

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© The Author(s) 2022

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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Bacterial SpxB mediated the activation of Nrf2-ARE. The amount of H₂O₂ produced by wild-type, ΔspxB mutants and ΔspxB complemented mutant (ΔspxB + pSpxB) of (a) S. mitis and (b) S. oralis were measured. Raw 264.7 cells stably expressing the Nrf2-ARE SEAP reporter were infected with wild-type, ΔspxB mutants or ΔspxB complemented mutants of (c) S. mitis or (d) S. oralis. Cellular ARE activity was quantified by SEAP reporter assay. The expression of (e) HO-1 was determined by qRT-PCR. ***p < 0.001 compared to the control group.