title: DNA microarrays to study gene expression in allergic airways.
abstract: BACKGROUND
  Allergic rhinitis results from interactions between a large number of cells and mediators in different compartments of the body. DNA microarrays allow simultaneous measurement of expression of thousands of genes in the same tissue sample.
  
  
  OBJECTIVE
  To study gene expression in nasal mucosal biopsies from patients with allergic rhinitis using DNA micro-arrays.
  
  
  METHODS
  Nasal biopsies were obtained from 14 patients with symptomatic birch pollen-induced allergic rhinitis and five healthy controls. RNA was extracted from the biopsies and pooled into one patient pool and one control pool. These were analysed in duplicate with DNA micro-arrays containing more than 12 000 known genes.
  
  
  RESULTS
  Approximately half of the genes were expressed in the patient and control samples. Guided by the current literature we chose 32 genes of possible relevance to allergic airway inflammation and investigated their relative expression. Among these, transcripts encoding immunoglobulins and their receptors were most abundant. The expression of cytokines and growth factors was low, whereas their corresponding receptors and cell surface markers displayed higher expression levels. IgA had the highest expression of all 12 626 genes. RT-PCR showed that IgA1 was the predominant subclass. This was confirmed by the protein level in nasal fluids. Allergen-specific IgA was significantly higher in patients than in controls and correlated significantly with eosinophil granulae proteins.
  
  
  CONCLUSIONS
  DNA micro-array analysis can be used to identify genes of possible relevance to allergic airway inflammation. In this study, the expression profile in the nasal mucosa was quantitatively dominated by immunoglobulins, particularly IgA. Protein analyses in nasal fluids indicated a role for allergen-specific IgA in eosinophil degranulation.
authors.affiliation: Allergy Laboratory, Department of Oto-Rhino-Laryngology, Malmö University Hospital, S-205 02 Malmö, Sweden.
authors.forename: M
authors.initials: M
authors.lastname: Benson
authors.forename: P A
authors.initials: PA
authors.lastname: Svensson
authors.forename: B
authors.initials: B
authors.lastname: Carlsson
authors.forename: M
authors.initials: M
authors.lastname: Jernås
authors.forename: J
authors.initials: J
authors.lastname: Reinholdt
authors.forename: L O
authors.initials: LO
authors.lastname: Cardell
authors.forename: L
authors.initials: L
authors.lastname: Carlsson
mesh_terms: D000328:Adult; D001826:Body Fluids / Q000166:cytology / Q000378:metabolism; D002452:Cell Count; D015550:Cell Degranulation / Q000502:physiology; D004804:Eosinophils / Q000502:physiology; D015870:Gene Expression; D020869:Gene Expression Profiling / Q000379:methods*; D006801:Humans; D006967:Hypersensitivity / Q000235:genetics* / Q000503:physiopathology; D007070:Immunoglobulin A / Q000378:metabolism; D008875:Middle Aged; D009297:Nasal Mucosa / Q000503:physiopathology*; D020411:Oligonucleotide Array Sequence Analysis; D011506:Proteins / Q000378:metabolism; D012016:Reference Values
chemical_list: D007070:Immunoglobulin A; D011506:Proteins