title: Evaluation of the presence of B-cell attractant chemokines in chronic rhinosinusitis.
abstract: BACKGROUND
  B-cell responses may play a role in the pathogenesis of nasal polyposis via local IgA and IgE production and activation of eosinophils and mast cells. B-cell attracting chemokines may therefore have relevance in the pathogenesis of chronic rhinosinusitis with nasal polyps (CRSwNPs) Methods: Polyp and inferior turbinate tissues were obtained from CRSwNPs, CRS without NPs (CRSsNPs), and control patients; ELISA and reverse-transcription polymerase chain reaction were used to detect levels of protein and mRNA for selected B-cell chemokines (B-cell attracting chemokine 1 [CXCL13/BCA-1/BLC]), thymus expressed chemokine (CCL25/TECK), mucosae-associated epithelial chemokine (CCL28/MEC), stromal cell-derived factor-1alpha (CXCL12/SDF-1alpha), and selected chemokine receptor genes (CXCR4, CXCR5, and CXCR7).
  
  
  RESULTS
  BCA-1 and SDF-1alpha protein levels were significantly increased in polyp tissue compared with turbinate tissue from CRSsNP patients and controls (p < 0.05 and p < 0.01, respectively). Differences in TECK and MEC were not significant. For mRNA, expression of BCA-1 was significantly up-regulated in polyp tissue and levels correlated with CD20 mRNA expression. Additionally, significant up-regulation of mRNA for the SDF-1alpha receptors CXCR7 and CXCR4 was detected in polyps, while there was a trend for up-regulation of the BCA-1 receptor CXCR5.
  
  
  CONCLUSIONS
  Elevated levels of the BCA-1 and SDF-1alpha and their receptors may account for an increased presence of B cells and their products, contributing to eosinophilic inflammation in patients with CRSwNP.
authors.affiliation: Department of Otolaryngology, Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, Illinois, USA. mona33@gmail.com
authors.forename: Monica
authors.initials: M
authors.lastname: Patadia
authors.forename: Julian
authors.initials: J
authors.lastname: Dixon
authors.forename: David
authors.initials: D
authors.lastname: Conley
authors.forename: Rakesh
authors.initials: R
authors.lastname: Chandra
authors.forename: Anju
authors.initials: A
authors.lastname: Peters
authors.forename: Lydia A
authors.initials: LA
authors.lastname: Suh
authors.forename: Atsushi
authors.initials: A
authors.lastname: Kato
authors.forename: Roderick
authors.initials: R
authors.lastname: Carter
authors.forename: Kathleen
authors.initials: K
authors.lastname: Harris
authors.forename: Leslie
authors.initials: L
authors.lastname: Grammer
authors.forename: Robert
authors.initials: R
authors.lastname: Kern
authors.forename: Robert
authors.initials: R
authors.lastname: Schleimer
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D001402:B-Lymphocytes / Q000276:immunology; D054377:Chemokine CXCL12 / Q000235:genetics / Q000276:immunology / Q000378:metabolism*; D054382:Chemokine CXCL13 / Q000235:genetics / Q000276:immunology / Q000378:metabolism*; D002908:Chronic Disease; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009298:Nasal Polyps; D054387:Receptors, CXCR / Q000235:genetics / Q000276:immunology / Q000378:metabolism*; D019718:Receptors, CXCR4 / Q000235:genetics / Q000276:immunology / Q000378:metabolism*; D012220:Rhinitis; D012852:Sinusitis / Q000276:immunology* / Q000473:pathology / Q000503:physiopathology; D015854:Up-Regulation
chemical_list: C501896:ACKR3 protein, human; C515255:CXCL12 protein, human; C110663:CXCL13 protein, human; C527276:CXCR4 protein, human; D054377:Chemokine CXCL12; D054382:Chemokine CXCL13; D054387:Receptors, CXCR; D019718:Receptors, CXCR4