title: Neutrophil mobilization by surface-glycan altered Th17-skewing bacteria mitigates periodontal pathogen persistence and associated alveolar bone loss.
abstract: Alveolar bone (tooth-supporting bone) erosion is a hallmark of periodontitis, an inflammatory disease that often leads to tooth loss. Periodontitis is caused by a select group of pathogens that form biofilms in subgingival crevices between the gums and teeth. It is well-recognized that the periodontal pathogen Porphyromonas gingivalis in these biofilms is responsible for modeling a microbial dysbiotic state, which then initiates an inflammatory response destructive to the periodontal tissues and bone. Eradication of this pathogen is thus critical for the treatment of periodontitis. Previous studies have shown that oral inoculation in mice with an attenuated strain of the periodontal pathogen Tannerella forsythia altered in O-glycan surface composition induces a Th17-linked mobilization of neutrophils to the gingival tissues. In this study, we sought to determine if immune priming with such a Th17-biasing strain would elicit a productive neutrophil response against P. gingivalis. Our data show that inoculation with a Th17-biasing T. forsythia strain is effective in blocking P. gingivalis-persistence and associated alveolar bone loss in mice. This work demonstrates the potential of O-glycan modified Tannerella strains or their O-glycan components for harnessing Th17-mediated immunity against periodontal and other mucosal pathogens.
authors.affiliation: Department of Oral Biology, School of Dental Medicine, University at Buffalo, State University of New York, Buffalo, New York, United States of America.
authors.forename: Rajendra P
authors.initials: RP
authors.lastname: Settem
authors.affiliation: Department of Oral Biology, School of Dental Medicine, University at Buffalo, State University of New York, Buffalo, New York, United States of America.
authors.forename: Kiyonobu
authors.initials: K
authors.lastname: Honma
authors.affiliation: Department of Oral Biology, School of Dental Medicine, University at Buffalo, State University of New York, Buffalo, New York, United States of America.
authors.forename: Ashu
authors.initials: A
authors.lastname: Sharma
mesh_terms: D016301:Alveolar Bone Loss / Q000276:immunology*; D000818:Animals; D000907:Antibodies, Bacterial / Q000097:blood / Q000276:immunology; D001419:Bacteria / Q000276:immunology* / Q000378:metabolism*; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology / Q000378:metabolism; D002634:Chemotaxis, Leukocyte / Q000276:immunology; D016207:Cytokines / Q000096:biosynthesis; D004195:Disease Models, Animal; D005260:Female; D007074:Immunoglobulin G / Q000097:blood / Q000276:immunology; D051379:Mice; D020556:Neutrophil Infiltration / Q000276:immunology; D009504:Neutrophils / Q000276:immunology*; D010518:Periodontitis / Q000276:immunology* / Q000382:microbiology*; D011135:Polysaccharides, Bacterial / Q000276:immunology*; D016176:T-Lymphocyte Subsets / Q000276:immunology / Q000378:metabolism; D058504:Th17 Cells / Q000276:immunology*
chemical_list: D000907:Antibodies, Bacterial; D016207:Cytokines; D007074:Immunoglobulin G; D011135:Polysaccharides, Bacterial