title: Functional interferences in host inflammatory immune response by airway allergic inflammation restrain experimental periodontitis development in mice.
abstract: OBJECTIVE
  periodontal disease (PD) and airway allergic inflammation (AL) present opposing inflammatory immunological features and clinically present an inverse correlation. However, the putative mechanisms underlying such opposite association are unknown.
  
  
  METHODS
  Balb/C mice were submitted to the co-induction of experimental PD (induced by Actinobacillus actinomycetemcomitans oral inoculation) and AL [induced by sensitization with ovalbumin (OVA) and the subsequent OVA challenges], and evaluated regarding PD and AL severity, immune response [cytokine production at periodontal tissues, and T-helper transcription factors in submandibular lymph nodes (LNs)] and infection parameters.
  
  
  RESULTS
  PD/AL co-induction decreased PD alveolar bone loss and periodontal inflammation while experimental AL parameters were unaltered. An active functional interference was verified, because independent OVA sensitization and challenge not modulate PD outcome. PD+AL group presented decreased tumour necrosis factor-α (TNF-α), interleukin (IL)-1β, interferon-γ, IL-17A, receptor activator of nuclear factor κ-light-chain-enhancer of activated B cells ligand and matrix metalloproteinase (MMP)-13 levels in periodontal tissues, while IL-4 and IL-10 levels were unaltered by AL co-induction. AL co-induction also resulted in upregulated T-bet and related orphan receptor γ and downregulated GATA3 levels expression in submandibular LNs when compared with PD group.
  
  
  CONCLUSIONS
  our results demonstrate that the interaction between experimental periodontitis and allergy involves functional immunological interferences, which restrains experimental periodontitis development by means of a skewed immune response.
authors.affiliation: Department of Biochemistry and Immunology, School of Medicine of Ribeirão Preto - FMRP/USP, Ribeirão Preto, SP, Brazil.
authors.forename: Denise Morais
authors.initials: DM
authors.lastname: da Fonseca
authors.forename: Ana Paula Fávaro
authors.initials: AP
authors.lastname: Trombone
authors.forename: Carlos Eduardo
authors.initials: CE
authors.lastname: Repeke
authors.forename: Mario Julio
authors.initials: MJ
authors.lastname: Avila-Campos
authors.forename: Arlete A M
authors.initials: AA
authors.lastname: Coelho-Castelo
authors.forename: João Santana
authors.initials: JS
authors.lastname: Silva
authors.forename: Ana Paula
authors.initials: AP
authors.lastname: Campanelli
authors.forename: Vânia Luiza
authors.initials: VL
authors.lastname: Deperon Bonato
authors.forename: Gustavo Pompermaier
authors.initials: GP
authors.lastname: Garlet
mesh_terms: D000189:Actinobacillus Infections / Q000150:complications / Q000276:immunology* / Q000382:microbiology; D016976:Aggregatibacter actinomycetemcomitans / Q000276:immunology; D000818:Animals; D016207:Cytokines / Q000276:immunology*; D004198:Disease Susceptibility / Q000276:immunology; D055633:Immune System Phenomena; D018836:Inflammation Mediators / Q000276:immunology; D051379:Mice; D008807:Mice, Inbred BALB C; D010047:Ovalbumin; D010518:Periodontitis / Q000150:complications / Q000276:immunology* / Q000382:microbiology / Q000473:pathology; D010519:Periodontium / Q000276:immunology; D012130:Respiratory Hypersensitivity / Q000139:chemically induced / Q000150:complications / Q000276:immunology*; D012720:Severity of Illness Index; D013601:T-Lymphocytes / Q000276:immunology
chemical_list: D016207:Cytokines; D018836:Inflammation Mediators; D010047:Ovalbumin