title: Surfactant protein d expression in chronic rhinosinusitis patients and immune responses in vitro to Aspergillus and alternaria in a nasal explant model.
abstract: OBJECTIVE
  Common fungi have been implicated in the pathogenesis of chronic rhinosinusitis (CRS) with eosinophilic mucus (EMCRS). Surfactant protein (SP)-D plays an important role in the immune response to Aspergillus fumigatus in the lungs. We sought to determine whether SP-D is expressed in nasal mucosa and investigated the response of SP-D in vitro to fungal allergens.
  
  
  METHODS
  1) Nasal biopsies from 59 CRS and EMCRS patients, stratified into allergic fungal sinusitis (AFS), nonallergic fungal eosinophilic sinusitis (NAFES), and nonallergic nonfungal eosinophilic sinusitis (NANFES) were studied by quantitative reverse-transcriptase polymerase chain reaction (qRT-PCR), immunostaining and enzyme-linked immunosorbent assay (ELISA). 2) Nasal tissue from three CRS and three NANFES patients was cultured with fungal allergens in a nasal explant in vitro model for 24 hours at increasing concentrations and mRNA SP-D secreted SP-D protein levels in response to the fungi determined by qRT-PCR and ELISA.
  
  
  RESULTS
  Staining for SP-D was detected in the submucosal glands from the nasal biopsies in all patient groups except for AFS. By ELISA, SP-D was undetectable in AFS and decreased in NAFES, NANFES, and CRS compared with controls. CRS patients in vitro cultured with Aspergillus and Alternaria allergens in a nasal tissue explant model induced up-regulation of SP-D by qRT-PCR. In contrast, NANFES nasal tissue explants cultured with Aspergillus allergens induced down-regulation of SP-D.
  
  
  CONCLUSIONS
  We report for the first time the expression of SP-D in both diseased and normal nasal mucosa. SP-D expression in CRS patients is up-regulated by fungal allergens in an in vitro model. These results may provide potential novel therapy for treatment of CRS.
authors.affiliation: Department of Surgery-Otorhinolaryngology Head and Neck Surgery, University of Adelaide and Flinders University, South Australia.
authors.forename: Eng Hooi
authors.initials: EH
authors.lastname: Ooi
authors.forename: Peter-John
authors.initials: PJ
authors.lastname: Wormald
authors.forename: A Simon
authors.initials: AS
authors.lastname: Carney
authors.forename: Craig Lloyd
authors.initials: CL
authors.lastname: James
authors.forename: Lor Wai
authors.initials: LW
authors.lastname: Tan
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000485:Allergens / Q000276:immunology; D000528:Alternaria / Q000276:immunology*; D001232:Aspergillus fumigatus / Q000276:immunology*; D004802:Eosinophilia; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009093:Mucus / Q000276:immunology / Q000382:microbiology; D009297:Nasal Mucosa / Q000382:microbiology*; D011446:Prospective Studies; D037663:Pulmonary Surfactant-Associated Protein D / Q000096:biosynthesis* / Q000235:genetics; D012333:RNA, Messenger / Q000096:biosynthesis; D020133:Reverse Transcriptase Polymerase Chain Reaction; D012221:Rhinitis, Allergic, Perennial / Q000276:immunology / Q000378:metabolism* / Q000382:microbiology; D012852:Sinusitis / Q000276:immunology / Q000378:metabolism* / Q000382:microbiology; D015854:Up-Regulation
chemical_list: D000485:Allergens; D037663:Pulmonary Surfactant-Associated Protein D; D012333:RNA, Messenger