title: Allergen immunotherapy decreases LPS-induced NF-κB activation in neutrophils from allergic patients.
abstract: BACKGROUND
  Allergen-specific immunotherapy (IT) is widely used to treat allergic diseases. The molecular mechanisms have not been clarified yet completely. The present work was undertaken to analyze the effect of IT in the activation of NF-κB.
  
  
  METHODS
  Neutrophils from 15 pollen-allergic IT-treated patients, 10 untreated pollen-allergic patients, and 10 healthy donors were in vitro stimulated with LPS. NF-κB activation (p65/p52) was measured in their nuclear extracts by enzyme-linked immunosorbent assay (ELISA). IκBα phosphorylation, NF-κB-repressing factor (NRF) activation, and thromboxane A2 (TXA2 ) and Interleukin-8 (IL-8) release were measured by ELISA.
  
  
  RESULTS
  There was a positive correlation between the score of symptoms and NF-κB activation in human neutrophils. IT significantly decreased NF-κB activation levels in neutrophils compared with neutrophils from untreated patients. IκBα phosphorylation and NRF activation levels were, respectively, significantly lower and higher in neutrophils from IT-treated patients than from untreated patients. IL-8 and TXA2 release were significantly lower in neutrophils from IT-treated patients than from untreated patients.
  
  
  CONCLUSIONS
  IT positive effects are at least in part mediated by the negative regulation of NF-κB activation in human neutrophils. These observations represent a novel view of neutrophils as possible cell target to treat IgE-dependent diseases through NF-κB downmodulation.
authors.affiliation: Servicio de Inmunología y Alergia, Hospital Universitario Virgen Macarena, Sevilla, Spain.
authors.forename: Inmaculada
authors.initials: I
authors.lastname: Ventura
authors.forename: Antonio
authors.initials: A
authors.lastname: Vega
authors.forename: Cristina
authors.initials: C
authors.lastname: Chamorro
authors.forename: Rocío
authors.initials: R
authors.lastname: Aroca
authors.forename: Elisa
authors.initials: E
authors.lastname: Gómez
authors.forename: Fernando
authors.initials: F
authors.lastname: Pineda
authors.forename: Ricardo
authors.initials: R
authors.lastname: Palacios
authors.forename: Miguel
authors.initials: M
authors.lastname: Blanca
authors.forename: Javier
authors.initials: J
authors.lastname: Monteseirín
mesh_terms: D000293:Adolescent; D000485:Allergens / Q000627:therapeutic use*; D016022:Case-Control Studies; D002478:Cells, Cultured; D031745:Dactylis / Q000276:immunology*; D003888:Desensitization, Immunologic / Q000379:methods*; D015536:Down-Regulation; D005260:Female; D006801:Humans; D020672:I-kappa B Proteins / Q000378:metabolism; D018836:Inflammation Mediators / Q000378:metabolism*; D016209:Interleukin-8 / Q000378:metabolism; D008070:Lipopolysaccharides / Q000494:pharmacology*; D008297:Male; D000072000:NF-KappaB Inhibitor alpha; D016328:NF-kappa B / Q000378:metabolism*; D052003:NF-kappa B p52 Subunit / Q000378:metabolism; D009504:Neutrophils / Q000187:drug effects* / Q000276:immunology / Q000378:metabolism; D010766:Phosphorylation; D011058:Pollen / Q000276:immunology*; D012097:Repressor Proteins / Q000378:metabolism; D006255:Rhinitis, Allergic, Seasonal / Q000175:diagnosis / Q000276:immunology / Q000628:therapy*; D015398:Signal Transduction / Q000187:drug effects; D013928:Thromboxane A2 / Q000378:metabolism; D051996:Transcription Factor RelA / Q000378:metabolism; D016896:Treatment Outcome
chemical_list: D000485:Allergens; C508606:CXCL8 protein, human; D020672:I-kappa B Proteins; D018836:Inflammation Mediators; D016209:Interleukin-8; D008070:Lipopolysaccharides; D016328:NF-kappa B; D052003:NF-kappa B p52 Subunit; C000606204:NFKBIA protein, human; C111027:NKRF protein, human; C498143:RELA protein, human; D012097:Repressor Proteins; D051996:Transcription Factor RelA; D000072000:NF-KappaB Inhibitor alpha; D013928:Thromboxane A2
keywords: NF-κB; allergen immunotherapy; asthma; neutrophils