title: Role of Porphyromonas gingivalis phosphoserine phosphatase enzyme SerB in inflammation, immune response, and induction of alveolar bone resorption in rats.
abstract: Porphyromonas gingivalis secretes a serine phosphatase enzyme, SerB, upon contact with gingival epithelial cells in vitro. The SerB protein plays a critical role in internalization and survival of the organism in epithelial cells. SerB is also responsible for the inhibition of interleukin-8 (IL-8) secretion from gingival epithelial cells infected with P. gingivalis. This study examined the ability of a P. gingivalis SerB mutant to colonize the oral cavity and induce gingival inflammation, immune responses, and alveolar bone resorption in a rat model of periodontal disease. Both P. gingivalis ATCC 33277 and an isogenic ΔSerB mutant colonized the oral cavities of rats during the 12-week experimental period. Both of the strains induced significant (P < 0.05) systemic levels of immunoglobulin G (IgG) and isotypes IgG1, IgG2a, and IgG2b, indicating the involvement of both T helper type 1 (Th1) and Th2 responses to infection. Both strains induced significantly (P < 0.05) higher levels of alveolar bone resorption in infected rats than in sham-infected control rats. However, horizontal and interproximal alveolar bone resorption induced by the SerB mutant was significantly (P < 0.05) lower than that induced by the parental strain. Rats infected with the ΔSerB mutant exhibited significantly higher levels of apical migration of the junctional epithelium (P < 0.01) and polymorphonuclear neutrophil (PMN) recruitment (P < 0.001) into the gingival tissues than rats infected with the wild type. In conclusion, in a rat model of periodontal disease, the SerB phosphatase of P. gingivalis is required for maximal alveolar bone resorption, and in the absence of SerB, more PMNs are recruited into the gingival tissues.
authors.affiliation: Department of Oral Biology, College of Dentistry, University of Florida, Gainesville, FL 32610, USA.
authors.forename: Brian
authors.initials: B
authors.lastname: Bainbridge
authors.forename: Raj K
authors.initials: RK
authors.lastname: Verma
authors.forename: Christie
authors.initials: C
authors.lastname: Eastman
authors.forename: Bilal
authors.initials: B
authors.lastname: Yehia
authors.forename: Mercedes
authors.initials: M
authors.lastname: Rivera
authors.forename: Catherine
authors.initials: C
authors.lastname: Moffatt
authors.forename: Indraneel
authors.initials: I
authors.lastname: Bhattacharyya
authors.forename: Richard J
authors.initials: RJ
authors.lastname: Lamont
authors.forename: Lakshmyya
authors.initials: L
authors.lastname: Kesavalu
mesh_terms: D016301:Alveolar Bone Loss / Q000276:immunology / Q000382:microbiology* / Q000473:pathology; D000818:Animals; D000907:Antibodies, Bacterial / Q000097:blood; D016866:Bacteroidaceae Infections / Q000276:immunology / Q000382:microbiology* / Q000473:pathology; D004195:Disease Models, Animal; D005260:Female; D006801:Humans; D007074:Immunoglobulin G / Q000097:blood; D007249:Inflammation / Q000276:immunology / Q000382:microbiology / Q000473:pathology; D010510:Periodontal Diseases / Q000276:immunology / Q000382:microbiology* / Q000473:pathology; D010744:Phosphoric Monoester Hydrolases / Q000235:genetics / Q000378:metabolism*; D016966:Porphyromonas gingivalis / Q000201:enzymology / Q000235:genetics / Q000276:immunology / Q000472:pathogenicity*; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D000907:Antibodies, Bacterial; D007074:Immunoglobulin G; D010744:Phosphoric Monoester Hydrolases; C022394:phosphoserine phosphatase
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