title: Th2 cytokines differentially regulate psoriasin expression in human nasal epithelia.
abstract: BACKGROUND
  Psoriasin is known to be expressed in diverse organs, where it exerts antimicrobial activity. Psoriasin is also involved in the local host defense mechanism against pathogens. We hypothesized that allergy-related T-helper cell type 2 (Th2) cytokines may regulate the expression of psoriasin.
  
  
  METHODS
  We treated normal human nasal epithelial (NHNE) cells with IL-4 or IL-13. Using human nasal tissues, we compared the expression level of psoriasin. We performed real-time polymerase chain reaction and Western blot assays using NHNE cells. Immunohistochemical staining and Western blot assays were performed with human nasal tissues. Furthermore, we studied the antimicrobial activity of nasal secretions from normal and allergic rhinitis patients.
  
  
  RESULTS
  IL-13 markedly down-regulated psoriasin expression at the gene and protein levels in NHNE cells, and it also decreased the amount of psoriasin protein that was secreted into the extracellular compartment in NHNE cells. IL-4 had no statistically significant effect. Results from immunohistochemical staining and Western blot assays showed that psoriasin expression was decreased in allergic rhinitis patients compared with control subjects. Nasal secretions of allergic rhinitis patients exhibited decreased antimicrobial activity compared with control subjects.
  
  
  CONCLUSIONS
  We found that Th2 cytokines regulated psoriasin expression in NHNE cells, and psoriasin expression was decreased in allergic rhinitis patients compared with control subjects. The decreased expression of psoriasin may be related to the reduction in antimicrobial capacity of nasal secretions under allergic conditions, resulting in an increase in susceptibility to viruses or bacterial infections.
authors.affiliation: Departmenrt of Otorhinolaryngology, Yonsei University College of Medicine, Seoul, Korea.
authors.forename: Hyun Jin
authors.initials: HJ
authors.lastname: Min
authors.forename: Hyuna
authors.initials: H
authors.lastname: Song
authors.forename: Su Yeon
authors.initials: SY
authors.lastname: Choi
authors.forename: Tae Hoon
authors.initials: TH
authors.lastname: Kim
authors.forename: Hyung-Ju
authors.initials: HJ
authors.lastname: Cho
authors.forename: Joo-Heon
authors.initials: JH
authors.lastname: Yoon
authors.forename: Chang-Hoon
authors.initials: CH
authors.lastname: Kim
mesh_terms: D000890:Anti-Infective Agents / Q000378:metabolism*; D002478:Cells, Cultured; D005786:Gene Expression Regulation / Q000276:immunology; D006801:Humans; D018793:Interleukin-13 / Q000276:immunology / Q000378:metabolism*; D015847:Interleukin-4 / Q000276:immunology / Q000378:metabolism; D009297:Nasal Mucosa / Q000276:immunology / Q000378:metabolism*; D065631:Rhinitis, Allergic / Q000276:immunology*; D000075023:S100 Calcium Binding Protein A7; D009418:S100 Proteins / Q000235:genetics / Q000378:metabolism*; D018418:Th2 Cells / Q000276:immunology
chemical_list: D000890:Anti-Infective Agents; D018793:Interleukin-13; D000075023:S100 Calcium Binding Protein A7; D009418:S100 Proteins; C089242:S100A7 protein, human; D015847:Interleukin-4