title: Innate immune system is implicated in recurrent aphthous ulcer pathogenesis.
abstract: BACKGROUND
  Recurrent aphthous ulcers (RAU) is a chronic inflammatory disease with evidence of inappropriate immune response. This study presents the status of innate immune system in RAU.
  
  
  METHODS
  Twenty RAU patients and 19 healthy individuals were selected. The status of peripheral blood neutrophils (reactive oxygen intermediates (ROI) production, CD11b, TNF-RI and TNF-RII expression), concentration of antioxidants, sTNF-R, C3c, C4 and haemolytic activity of the complement system, as well as mannose-binding lectin (MBL), in the serum of RAU patients in active stage and in remission of the disease were determined.
  
  
  RESULTS
  Peripheral blood neutrophils were primed in RAU, which resulted in increased ROI production by resting and fMLP-stimulated neutrophils and diminished ROI production after in vitro priming. The increased expression of CD11b on resting and fMLP-stimulated neutrophils in RAU may also point to their previous in vivo stimulation. The decreased total antioxidant status of serum observed in RAU may be a result of increased ROI production by peripheral blood neutrophils. The levels of C3c, C4 and haemolytic activity of the complement system were higher in RAU than in healthy people. No significant differences between active and remission RAU were noted.
  
  
  CONCLUSIONS
  Presented observations confirm that the innate immune system is involved in RAU pathogenesis.
authors.affiliation: Department of Oral Mucosal and Periodontal Diseases, Medical University of Lodz, Pomorska Str. 5, 9 - 1 Lodz, Poland. natalewk@wp.pl
authors.forename: Natalia
authors.initials: N
authors.lastname: Lewkowicz
authors.forename: Przemyslaw
authors.initials: P
authors.lastname: Lewkowicz
authors.forename: Anna
authors.initials: A
authors.lastname: Kurnatowska
authors.forename: Malgorzata
authors.initials: M
authors.lastname: Banasik
authors.forename: Ewa
authors.initials: E
authors.lastname: Glowacka
authors.forename: Maciej
authors.initials: M
authors.lastname: Cedzyński
authors.forename: Anna
authors.initials: A
authors.lastname: Swierzko
authors.forename: Bozena
authors.initials: B
authors.lastname: Lauk-Puchala
authors.forename: Henryk
authors.initials: H
authors.lastname: Tchórzewski
mesh_terms: D000293:Adolescent; D000328:Adult; D015703:Antigens, CD / Q000097:blood; D000975:Antioxidants / Q000032:analysis; D017209:Apoptosis / Q000276:immunology; D039481:CD11b Antigen / Q000097:blood; D015932:Complement C3c / Q000032:analysis; D003181:Complement C4 / Q000032:analysis; D000068800:Etanercept; D005260:Female; D006461:Hemolysis; D006801:Humans; D007074:Immunoglobulin G / Q000097:blood; D007155:Immunologic Factors / Q000097:blood; D008297:Male; D037601:Mannose-Binding Lectin / Q000097:blood; D008875:Middle Aged; D018375:Neutrophil Activation / Q000276:immunology; D009504:Neutrophils / Q000276:immunology; D017382:Reactive Oxygen Species / Q000097:blood; D018124:Receptors, Tumor Necrosis Factor / Q000097:blood; D047888:Receptors, Tumor Necrosis Factor, Type I; D047889:Receptors, Tumor Necrosis Factor, Type II; D012008:Recurrence; D013281:Stomatitis, Aphthous / Q000097:blood / Q000276:immunology*
chemical_list: D015703:Antigens, CD; D000975:Antioxidants; D039481:CD11b Antigen; D003181:Complement C4; D007074:Immunoglobulin G; D007155:Immunologic Factors; D037601:Mannose-Binding Lectin; D017382:Reactive Oxygen Species; D018124:Receptors, Tumor Necrosis Factor; D047888:Receptors, Tumor Necrosis Factor, Type I; D047889:Receptors, Tumor Necrosis Factor, Type II; D015932:Complement C3c; D000068800:Etanercept