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. 2023 Apr 2;15(1):2197779. doi: 10.1080/20002297.2023.2197779

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© 2023 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The terms on which this article has been published allow the posting of the Accepted Manuscript in a repository by the author(s) or with their consent.

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Figure 8. — Porphyromonas gingivalis-induced chemokine paralysis. The activated Toll-like receptors (TLR), following interaction with oral pathobionts such as Fusobacterium nucleatum, induce proinflammatory signaling mechanisms. The invading keystone pathogen (P. gingivalis) can suppress interleukin (IL)-8 production through dephosphorylation of S536 residue of p65 subunit of nuclear factor kappa B (NF-kB) by the activity of serine phosphatase B (SerB), disrupting neutrophil recruitment. Similarly, the expression of chemokine CXCL9 (Mig), CXCL10 (IP-10), and CXCL11 (ITAC) could be inhibited through blocking the signal transducer and activator of transcription 1 (STAT1)-interferon regulatory factor 1 (IRF1) pathway by P. gingivalis, leading to T cell imbalance, including TH17 activation (IL-6, IL-23) and TH1 suppression (IL-12). These immune subversion mechanisms lead to enhanced inflammatory responses and dysbiosis.