{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,30]],"date-time":"2025-10-30T11:39:08Z","timestamp":1761824348651,"version":"3.41.2"},"reference-count":22,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2022,1,20]],"date-time":"2022-01-20T00:00:00Z","timestamp":1642636800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["81970942","81800974"],"award-info":[{"award-number":["81970942","81800974"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["European J Oral Sciences"],"published-print":{"date-parts":[[2022,4]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p><jats:italic>Porphyromonas gingivalis<\/jats:italic> is the main pathogen of chronic periodontitis. However, the specific mechanisms through which <jats:italic>P. gingivalis<\/jats:italic> induces immune and inflammatory responses in periodontitis have not been completely elucidated. In this study, we investigated the effects of the <jats:italic>P. gingivalis<\/jats:italic> outer membrane protein OmpH (encoded by PG0192 and PG0193) on interleukin\u20106 (IL\u20106) and tumor necrosis factor\u2010\u03b1 (TNF\u2010\u03b1) expression in macrophages to assess the pro\u2010inflammatory cytokine responses. A PG0192\u2010PG0193 deletion mutant strain and a com\u25b3PG0192\u20100193 strain were constructed. Furthermore, rOmpH\u20101 and rOmpH\u20102 encoded by PG0192 and PG0193, respectively, were cloned, expressed, and purified for subsequent experiments. Notably, the expression of IL\u20106 and TNF\u2010\u03b1 at mRNA and protein levels was downregulated upon treatment of macrophages with the PG0192\u2010PG0193 deletion mutant strain, whereas treatment of macrophages with <jats:italic>P. gingivalis<\/jats:italic> W83 co\u2010incubated with rOmpH\u20101 or rOmpH\u20102 upregulated <jats:italic>IL\u20106<\/jats:italic> and <jats:italic>TNF\u2010\u03b1<\/jats:italic> mRNA levels. The addition of C5aR antagonist blocked this induction. Overall, our findings provided important insights into the roles of PG0192 and PG0193 for promoting IL\u20106 and TNF\u2010\u03b1 expression in macrophages exposed to <jats:italic>P. gingivalis<\/jats:italic> and revealed the involvement of C5aR in the pro\u2010inflammatory response.<\/jats:p>","DOI":"10.1111\/eos.12851","type":"journal-article","created":{"date-parts":[[2022,1,20]],"date-time":"2022-01-20T11:23:44Z","timestamp":1642677824000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["Role of PG0192 and PG0193 in the modulation of pro\u2010inflammatory cytokines in macrophages in response to <i>Porphyromonas gingivalis<\/i>"],"prefix":"10.1111","volume":"130","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-4745-2760","authenticated-orcid":false,"given":"Hongyan","family":"Wang","sequence":"first","affiliation":[{"name":"Department of Periodontology School of Stomatology China Medical University  Shenyang 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