{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T01:13:30Z","timestamp":1787015610109,"version":"build-2736575974"},"reference-count":45,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2019,4,14]],"date-time":"2019-04-14T00:00:00Z","timestamp":1555200000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/100000072","name":"National Institute of Dental and Craniofacial Research","doi-asserted-by":"publisher","award":["R01DE017680"],"award-info":[{"award-number":["R01DE017680"]}],"id":[{"id":"10.13039\/100000072","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000072","name":"National Institute of Dental and Craniofacial Research","doi-asserted-by":"publisher","award":["R01DE019826"],"award-info":[{"award-number":["R01DE019826"]}],"id":[{"id":"10.13039\/100000072","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000057","name":"National Institute of General Medical Sciences","doi-asserted-by":"publisher","award":["P20GM125504"],"award-info":[{"award-number":["P20GM125504"]}],"id":[{"id":"10.13039\/100000057","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J of Periodontal Research"],"published-print":{"date-parts":[[2019,10]]},"abstract":"<jats:sec>\n                    <jats:title>Objectives<\/jats:title>\n                    <jats:p>We hypothesized that short chain fatty acid (SCFA) production by oral pathogens is suppressed by exposure to cigarette smoke extract (CSE).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Tobacco smoking is a major risk factor for plaque\u2010induced periodontal diseases. Despite increased disease susceptibility, overt oral inflammation is suppressed in smokers, presenting a diagnostic conundrum. Bacterial\u2010derived SCFAs can penetrate into oral tissues where they influence multiple components of immune and healing responses. Indeed, the SCFA burden has been correlated with the inflammatory condition of the gingiva. However, the influence of cigarette consumption on SCFA production is unknown.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      GC\/MS was employed to monitor the production of several SCFAs (propionic acid, isobutyric acid, butyric acid, and isovaleric acid) by representative anaerobic oral pathogens (\n                      <jats:italic>Filifactor alocis<\/jats:italic>\n                      35896,\n                      <jats:italic>Fusobacterium nucleatum<\/jats:italic>\n                      25586,\n                      <jats:italic>Porphyromonas gingivalis<\/jats:italic>\n                      33277) that were exposed, or not, to a physiologically relevant dose of CSE (2000\u00a0ng\/ml nicotine equivalents) generated from 3R4F reference cigarettes.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      The growth of all three bacterial species was unaffected by CSE. The capacity to produce SCFAs by these bacteria was highly varied.\n                      <jats:italic>F\u00a0alocis<\/jats:italic>\n                      produced the highest concentration of a specific SCFA (butyrate);\n                      <jats:italic>P\u00a0gingivalis<\/jats:italic>\n                      provided the most robust overall SCFA signal, while\n                      <jats:italic>F\u00a0alocis<\/jats:italic>\n                      and\n                      <jats:italic>F\u00a0nucleatum<\/jats:italic>\n                      did not release detectable levels of isobutyrate or isovalerate. As\n                      <jats:italic>P\u00a0gingivalis<\/jats:italic>\n                      33277 was the broadest SCFA producer, three low\u2010passage clinical isolates (10208C, 5607, and 10512) were also examined. Compared to unconditioned microbes, reduced SCFA release was apparent in CSE\u2010exposed low\u2010passage clinical isolates of\n                      <jats:italic>P\u00a0gingivalis<\/jats:italic>\n                      which reached significance for one of the three isolates (propionic, isobutyric, butyric, and isovaleric acids, all\n                      <jats:italic>P<\/jats:italic>\n                      \u00a0&lt;\u00a00.05).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>\n                      There is high disparity in the SCFA profiles of variant chronic periodontitis\u2010associated bacteria, while CSE exposure reduces SCFA production by a specific clinical strain of\n                      <jats:italic>P\u00a0gingivalis<\/jats:italic>\n                      . If the latter phenomenon occurs in vivo, a reduced SCFA burden may help explain the reduced vascular response to dental plaque in tobacco smokers.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/jre.12660","type":"journal-article","created":{"date-parts":[[2019,4,15]],"date-time":"2019-04-15T02:38:17Z","timestamp":1555295897000},"page":"566-571","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":19,"title":["Cigarette smoke reduces short chain fatty acid production by a\n                    <i>Porphyromonas gingivalis<\/i>\n                    clinical isolate"],"prefix":"10.1111","volume":"54","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-3272-9835","authenticated-orcid":false,"given":"Iris","family":"Zeller","sequence":"first","affiliation":[{"name":"Departments of Oral Immunology and Infectious Diseases University of Louisville Louisville 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Kentucky"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1007-2756","authenticated-orcid":false,"given":"David A.","family":"Scott","sequence":"additional","affiliation":[{"name":"Departments of Oral Immunology and Infectious Diseases University of Louisville Louisville 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