title: Alterations in gene expression of complement components in chronic rhinosinusitis.
abstract: BACKGROUND
  The complement cascade forms part of the initial innate response to pathogens in the airway. Complement activation is important in the maintenance of host homeostasis, but excessive and uncontrolled activation may lead to inflammation and disease. The role of the complement pathway in the innate response in chronic rhinosinusitis (CRS) is poorly characterized Methods: Sinus mucosa biopsy specimens from the anterior ethmoid or uncinate process of patients with allergic fungal rhinosinusitis (AFRS), CRS without NPs (CRS-NPs), and controls were harvested and gene and protein expression of C3, factor B (fB), C5, and C7 complement proteins were analyzed using quantitative polymerase chain reaction and immunohistochemical techniques.
  
  
  RESULTS
  fB, C3, and C5 gene expression were increased in both AFRS and CRS-NPs compared with controls (p < 0.05). Transcriptional activity for the terminal pathway protein C7 was not significantly increased when compared with controls, with C7 levels actually reduced in AFRS patients when compared with controls. Immunohistochemistry studies showed the presence of C3 and fB on the mucosal surface and in submucosa of both AFRS and CRS-NPs, but not normal controls. Terminal pathway protein C9 was not found in our specimens.
  
  
  CONCLUSIONS
  Both AFRS and CRS-NPs display up-regulation of the complement pathway, in particular, the alternative pathway (fB) and common pathways (C3 and C5). Enhanced innate responses as shown by alterations in complement components may play a pivotal role in the inflammatory response noted in CRS and provide potential therapeutic targets in the future.
authors.affiliation: Department of Otolaryngology-Head and Neck Surgery, Medical University of South Carolina, Charleston, South Carolina, USA. schlossr@musc.edu
authors.forename: Rodney J
authors.initials: RJ
authors.lastname: Schlosser
authors.forename: Ryan M
authors.initials: RM
authors.lastname: Mulligan
authors.forename: Sarah E
authors.initials: SE
authors.lastname: Casey
authors.forename: Juan C
authors.initials: JC
authors.lastname: Varela
authors.forename: Richard J
authors.initials: RJ
authors.lastname: Harvey
authors.forename: Carl
authors.initials: C
authors.lastname: Atkinson
mesh_terms: D002908:Chronic Disease; D003165:Complement System Proteins / Q000235:genetics / Q000276:immunology / Q000378:metabolism*; D005658:Fungi / Q000276:immunology* / Q000472:pathogenicity; D005786:Gene Expression Regulation / Q000276:immunology; D006801:Humans; D007150:Immunohistochemistry; D009181:Mycoses / Q000150:complications / Q000276:immunology*; D009297:Nasal Mucosa / Q000276:immunology / Q000378:metabolism; D009298:Nasal Polyps; D020133:Reverse Transcriptase Polymerase Chain Reaction; D012221:Rhinitis, Allergic, Perennial / Q000209:etiology / Q000276:immunology* / Q000503:physiopathology; D012852:Sinusitis / Q000209:etiology / Q000276:immunology* / Q000503:physiopathology
chemical_list: D003165:Complement System Proteins