title: Bacteroides-specific IgG and IgA subclass antibody-secreting cells isolated from chronically inflamed gingival tissues.
abstract: The emergence of cells that produce IgG and IgA subclass antibodies to Bacteroides gingivalis (Porphyromonas gingivalis) fimbriae and lipopolysaccharide (LPS) antigens was examined in mononuclear cells isolated from inflamed gingiva of different stages (slight, moderate or advanced) of adult periodontitis (AP). Antigen-specific IgM, IgG (including IgG1, IgG2, IgG3 and IgG4) and IgA (including IgA1 and IgA2) producing cells were enumerated by the ELISPOT assay and were compared with total Ig-producing cells of each isotype or subclass. In advanced AP, the B. gingivalis fimbriae-specific IgG- and IgA-secreting cells represented 5% of total IgG- or IgA-secreting cells, while those from the moderate stage comprised approximately 1% of these two isotypes. Cells producing antibody specific for B. gingivalis LPS were observed at frequencies of 0.1% and 0.4% for IgG and IgA cells, respectively in the advanced stage. When IgG subclasses were analysed in moderate AP, the anti-fimbriae subclass responses were largely IgG1 (60%), followed by IgG2 (20%), IgG3 (10%) and IgG4 (10%). Fimbriae-specific IgG subclass responses were elevated in the advanced stage of AP, and IgG4 (40%) and IgG1 (30%) were dominant, followed by IgG3 (20%) and IgG2 (10%). IgA1 cells predominated in both the moderate and advanced stages, however a relative increase in IgA2 cells occurred in advanced AP. Mononuclear cells isolated from gingiva of AP patients did not contain cells producing antibody to antigens such as Escherichia coli K235 LPS, cholera toxin or the hapten dinitrophenyl coupled to bovine serum albumin. These results show that local IgG and IgA subclass responses occur to a protein antigen of a major periodontal disease (PD)-associated pathogen, B. gingivalis, and the increase in IgG4 and IgA2 responses may be associated with host protection.
authors.affiliation: Department of Oral Biology, University of Alabama, Birmingham 35294.
authors.forename: T
authors.initials: T
authors.lastname: Ogawa
authors.forename: M L
authors.initials: ML
authors.lastname: McGhee
authors.forename: Z
authors.initials: Z
authors.lastname: Moldoveanu
authors.forename: S
authors.initials: S
authors.lastname: Hamada
authors.forename: J
authors.initials: J
authors.lastname: Mestecky
authors.forename: J R
authors.initials: JR
authors.lastname: McGhee
authors.forename: H
authors.initials: H
authors.lastname: Kiyono
mesh_terms: D000907:Antibodies, Bacterial / Q000145:classification; D000921:Antibody-Producing Cells / Q000276:immunology*; D001439:Bacteroides / Q000276:immunology*; D010861:Fimbriae, Bacterial / Q000276:immunology; D005881:Gingiva / Q000276:immunology*; D005891:Gingivitis / Q000276:immunology; D006801:Humans; D007070:Immunoglobulin A / Q000145:classification*; D007074:Immunoglobulin G / Q000145:classification*; D010518:Periodontitis / Q000276:immunology
chemical_list: D000907:Antibodies, Bacterial; D007070:Immunoglobulin A; D007074:Immunoglobulin G