{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"institution":[{"name":"bioRxiv"}],"indexed":{"date-parts":[[2026,5,11]],"date-time":"2026-05-11T13:10:34Z","timestamp":1778505034556,"version":"3.51.4"},"posted":{"date-parts":[[2026,5,6]]},"group-title":"Microbiology","reference-count":50,"publisher":"openRxiv","license":[{"start":{"date-parts":[[2026,5,6]],"date-time":"2026-05-06T00:00:00Z","timestamp":1778025600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/www.biorxiv.org\/about\/FAQ#license"}],"funder":[{"DOI":"10.13039\/100000072","name":"National Institute of Dental and Craniofacial Research","doi-asserted-by":"crossref","award":["R01DE033659"],"award-info":[{"award-number":["R01DE033659"]}],"id":[{"id":"10.13039\/100000072","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/100000072","name":"National Institute of Dental and Craniofacial Research","doi-asserted-by":"crossref","award":["R01DE031159"],"award-info":[{"award-number":["R01DE031159"]}],"id":[{"id":"10.13039\/100000072","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"accepted":{"date-parts":[[2026,5,6]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                <jats:p>\n                  Periodontal disease is an inflammatory disorder that arises from dysbiosis of the subgingival microbiota, with\n                  <jats:italic>Porphyromonas gingivalis<\/jats:italic>\n                  acting as a keystone pathogen in the shift from health to disease.\n                  <jats:italic>P. gingivalis<\/jats:italic>\n                  employs multiple strategies to subvert host immune defenses, and its capsular K-antigen serves as a key virulence determinant. Here, a pre-adsorbed antiserum (pAds106) was generated by removing nonspecific antibodies using cells from a K-antigen\u2013null mutant (W83\u0394PG0106), resulting in exceptional specificity for the\n                  <jats:italic>P. gingivalis<\/jats:italic>\n                  K1-antigen. Immunofluorescence analysis revealed that the K-antigen preferentially coats outer membrane vesicles (OMVs), rather than attaching to the bacterial cell surface. This localization was further confirmed by ELISAs of density gradient ultracentrifuge-purified OMVs, with background signal detected in OMVs derived from K-antigen-deficient strains, non-K1-strains, and other oral Bacteroidetes. K-antigen\u2013coated OMVs exhibited higher hydrophilicity and elicited weaker inflammatory responses compared to K-antigen\u2013deficient OMVs, consistent with previously reported properties of encapsulated strains. Importantly, the antiserum detected K-antigen-coated OMVs in subgingival plaque from periodontal patients, suggesting that K-antigen is actively produced at diseased sites. These findings revise the prevailing view that K-antigen solely encapsulates the bacterial cell body and suggest that K-antigen\u2013coated OMVs produced by\n                  <jats:italic>P. gingivalis<\/jats:italic>\n                  play distinct roles in immune evasion during periodontal disease.\n                <\/jats:p>","DOI":"10.64898\/2026.05.05.723094","type":"posted-content","created":{"date-parts":[[2026,5,7]],"date-time":"2026-05-07T07:55:18Z","timestamp":1778140518000},"source":"Crossref","is-referenced-by-count":0,"title":["Capsular K-antigen Coats Outer Membrane Vesicles of\n                  <i>Porphyromonas gingivalis<\/i>"],"prefix":"10.64898","author":[{"given":"Hyun Young","family":"Kim","sequence":"first","affiliation":[{"name":"Department of Microbiology, ADA Forsyth Institute, Somerville, Massachusetts, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yeon Kyeong","family":"Ko","sequence":"additional","affiliation":[{"name":"Department of Microbiology, ADA Forsyth Institute, Somerville, Massachusetts, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hatice","family":"Hasturk","sequence":"additional","affiliation":[{"name":"Center for Clinical and Translational Research, ADA Forsyth Institute, Somerville, Massachusetts, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"suffix":"III","given":"Frank C.","family":"Gibson","sequence":"additional","affiliation":[{"name":"Department of Oral Biology, College of Dentistry, University of Florida, Gainesville, Florida, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5932-9597","authenticated-orcid":false,"given":"Manda","family":"Yu","sequence":"additional","affiliation":[{"name":"Department of Microbiology, ADA Forsyth Institute, Somerville, Massachusetts, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Mary Ellen","family":"Davey","sequence":"additional","affiliation":[{"name":"Department of Microbiology, ADA Forsyth Institute, Somerville, Massachusetts, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"54368","reference":[{"key":"2026051105250442000_2026.05.05.723094v1.1","doi-asserted-by":"publisher","DOI":"10.3389\/fmicb.2020.00432"},{"key":"2026051105250442000_2026.05.05.723094v1.2","doi-asserted-by":"publisher","DOI":"10.3947\/ic.2022.0145"},{"key":"2026051105250442000_2026.05.05.723094v1.3","doi-asserted-by":"publisher","DOI":"10.1038\/nrmicro3525"},{"key":"2026051105250442000_2026.05.05.723094v1.4","doi-asserted-by":"publisher","DOI":"10.1371\/journal.ppat.1005672"},{"key":"2026051105250442000_2026.05.05.723094v1.5","doi-asserted-by":"publisher","DOI":"10.1128\/JB.00257-06"},{"key":"2026051105250442000_2026.05.05.723094v1.6","doi-asserted-by":"publisher","DOI":"10.1128\/mbio.03304-23"},{"issue":"1","key":"2026051105250442000_2026.05.05.723094v1.7","doi-asserted-by":"crossref","first-page":"1340085","DOI":"10.1080\/20002297.2017.1340085","article-title":"Porphyromonas gingivalis disturbs host-commensal homeostasis by changing complement function","volume":"9","year":"2017","journal-title":"J Oral Microbiol"},{"key":"2026051105250442000_2026.05.05.723094v1.8","doi-asserted-by":"publisher","DOI":"10.1038\/nrmicro2873"},{"key":"2026051105250442000_2026.05.05.723094v1.9","doi-asserted-by":"crossref","first-page":"987683","DOI":"10.3389\/fcimb.2022.987683","article-title":"Implications of Porphyromonas gingivalis peptidyl arginine deiminase and gingipain R in human health and diseases","volume":"12","year":"2022","journal-title":"Frontiers in cellular and infection microbiology"},{"issue":"1","key":"2026051105250442000_2026.05.05.723094v1.10","doi-asserted-by":"crossref","first-page":"1440128","DOI":"10.1080\/20002297.2018.1440128","article-title":"Importance of heterogeneity in Porhyromonas gingivalis lipopolysaccharide lipid A in tissue specific inflammatory signalling","volume":"10","year":"2018","journal-title":"J Oral Microbiol"},{"key":"2026051105250442000_2026.05.05.723094v1.11","doi-asserted-by":"publisher","DOI":"10.1016\/j.jdsr.2021.07.003"},{"key":"2026051105250442000_2026.05.05.723094v1.12","doi-asserted-by":"crossref","unstructured":"Rocha FG , Ottenberg G , Eure ZG , Davey ME , & Gibson FC, 3rd (2021) Sphingolipid-Containing Outer Membrane Vesicles Serve as a Delivery Vehicle To Limit Macrophage Immune Response to Porphyromonas gingivalis. 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