title: LPS-induced inflammatory response after therapy of aggressive periodontitis.
abstract: We have reported a lipopolysaccharide (LPS)-induced hyper-inflammatory response in localized aggressive periodontitis (LAP). It is unknown whether treatment is able to modulate this LPS responsiveness. Fifty-nine individuals with LAP were treated by mechanical debridement and systemic antibiotics. Clinical parameters and cyto/chemokine responsiveness of whole blood stimulated with Porphyromonas gingivalis or Escherichia coli LPS were monitored at baseline and 3, 6, and 12 months post-treatment. Overall, clinical parameters were improved following treatment. Additionally, P. gingivalis LPS induction of eotaxin, IFNγ, IL10, IL12p40, IL1β, IL6, IP10, MCP1, MIP1α, GM-CSF, and TNFα was significantly decreased (p < .05). Similarly, induction of eotaxin, INFγ, IL10, IL12p40, GM-CSF, and TNFα by E. coli LPS was also reduced post-treatment. These reductions correlated with decreases in clinical parameters. Importantly, these reductions in LPS responsiveness were most robust at 3 months, and some lost significance at 6 to 12 months post-treatment. In conclusion, LPS-induced hyper-inflammatory response in LAP can be partially modulated by periodontal therapy. Conversely, rebound in the hyper-responsiveness of some mediators, in the presence of improved clinical parameters, suggests that this phenotype could be partially influenced by a genetic trait and play a role in future disease recurrence (ClinicalTrials.gov, NCT01330719).
authors.affiliation: Department of Periodontology, University of Florida College of Dentistry, Gainesville, FL, USA. lshaddox@dental.ufl.edu
authors.forename: L M
authors.initials: LM
authors.lastname: Shaddox
authors.forename: P F
authors.initials: PF
authors.lastname: Gonçalves
authors.forename: A
authors.initials: A
authors.lastname: Vovk
authors.forename: N
authors.initials: N
authors.lastname: Allin
authors.forename: H
authors.initials: H
authors.lastname: Huang
authors.forename: W
authors.initials: W
authors.lastname: Hou
authors.forename: I
authors.initials: I
authors.lastname: Aukhil
authors.forename: S M
authors.initials: SM
authors.lastname: Wallet
mesh_terms: D000293:Adolescent; D010520:Aggressive Periodontitis / Q000276:immunology / Q000628:therapy*; D000658:Amoxicillin / Q000627:therapeutic use; D000900:Anti-Bacterial Agents / Q000627:therapeutic use; D018932:Chemokine CCL2 / Q000032:analysis; D054405:Chemokine CCL3 / Q000032:analysis; D054357:Chemokine CXCL10 / Q000032:analysis; D019742:Chemokines, CC / Q000032:analysis; D002648:Child; D002675:Child, Preschool; D004926:Escherichia coli / Q000276:immunology; D005260:Female; D005500:Follow-Up Studies; D016178:Granulocyte-Macrophage Colony-Stimulating Factor / Q000032:analysis; D006801:Humans; D018836:Inflammation Mediators / Q000494:pharmacology*; D007371:Interferon-gamma / Q000032:analysis; D016753:Interleukin-10 / Q000032:analysis; D053762:Interleukin-12 Subunit p40 / Q000032:analysis; D053583:Interleukin-1beta / Q000032:analysis; D015850:Interleukin-6 / Q000032:analysis; D008070:Lipopolysaccharides / Q000494:pharmacology*; D008297:Male; D008795:Metronidazole / Q000627:therapeutic use; D017622:Periodontal Attachment Loss / Q000276:immunology / Q000628:therapy; D057747:Periodontal Debridement / Q000379:methods; D010514:Periodontal Pocket / Q000276:immunology / Q000628:therapy; D016966:Porphyromonas gingivalis / Q000276:immunology; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis; D055815:Young Adult
chemical_list: D000900:Anti-Bacterial Agents; C111835:CCL2 protein, human; C114753:CXCL10 protein, human; D018932:Chemokine CCL2; D054405:Chemokine CCL3; D054357:Chemokine CXCL10; D019742:Chemokines, CC; D018836:Inflammation Mediators; D053762:Interleukin-12 Subunit p40; D053583:Interleukin-1beta; D015850:Interleukin-6; D008070:Lipopolysaccharides; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D008795:Metronidazole; D000658:Amoxicillin; D007371:Interferon-gamma; D016178:Granulocyte-Macrophage Colony-Stimulating Factor
keywords: Escherichia coli; Porphyromonas gingivalis; TLR; chemokines; cytokines; immunity; inflammation