title: Increased CXCL10 expression in nasal fibroblasts from patients with refractory chronic rhinosinusitis and asthma.
abstract: BACKGROUND
  Chronic rhinosinusitis (CRS) is characterized by local inflammation of the sinonasal tissues. CRS patients with nasal polyps and asthma often develop acute exacerbation of sinonasal symptoms after upper respiratory tract infections. However, the influence of concomitant asthma on the nasal immune response to viral infection remains unclear.
  
  
  METHODS
  Specimens of nasal polyp and mucosal tissues were obtained from 3 groups of CRS patients (n = 14 per group): 1) patients without asthma (CRS group), 2) patients with aspirin-tolerant asthma (ATA group), and 3) patients with aspirin-intolerant asthma (AIA group). Nasal fibroblasts isolated from the specimens were stimulated with poly I:C. CXCL10 expression was analyzed by the quantitative real-time polymerase chain reaction and enzyme-linked immunoadsorbent assay. Biopsy specimens from CRS patients without asthma were subjected to immunohistochemistry for detection of T-bet and GATA-3 expression in CD3+ T cells by double labeling.
  
  
  RESULTS
  Nasal fibroblasts from the ATA and AIA groups showed significantly enhanced expression of CXCL10 mRNA and protein after poly I:C stimulation compared with cells from the CRS group and the control group (normal nasal mucosa). In addition to T helper (Th)2 cells, there was more abundant infiltration of Th1 cells into tissues from the AIA and ATA groups.
  
  
  CONCLUSIONS
  Our findings suggest that CRS associated with asthma may become intractable through the over-production of CXCL10 in response to viral infection.
authors.affiliation: Department of Otorhinolaryngology, Toho University School of Medicine, Tokyo, Japan.
authors.forename: Mamoru
authors.initials: M
authors.lastname: Yoshikawa
authors.forename: Kota
authors.initials: K
authors.lastname: Wada
authors.forename: Tsuyoshi
authors.initials: T
authors.lastname: Yoshimura
authors.forename: Daiya
authors.initials: D
authors.lastname: Asaka
authors.forename: Naoko
authors.initials: N
authors.lastname: Okada
authors.forename: Kenji
authors.initials: K
authors.lastname: Matsumoto
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Moriyama
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D001249:Asthma / Q000150:complications / Q000276:immunology*; D055963:Asthma, Aspirin-Induced / Q000150:complications / Q000276:immunology*; D017252:CD3 Complex / Q000378:metabolism; D002478:Cells, Cultured; D054357:Chemokine CXCL10 / Q000235:genetics / Q000378:metabolism*; D002908:Chronic Disease; D004351:Drug Resistance; D005260:Female; D005347:Fibroblasts / Q000276:immunology; D050990:GATA3 Transcription Factor / Q000378:metabolism; D006801:Humans; D008297:Male; D008875:Middle Aged; D009298:Nasal Polyps / Q000150:complications / Q000276:immunology*; D010256:Paranasal Sinuses / Q000276:immunology*; D011070:Poly I-C / Q000276:immunology; D012220:Rhinitis / Q000150:complications / Q000276:immunology*; D012852:Sinusitis / Q000150:complications / Q000276:immunology*; D020825:T-Box Domain Proteins / Q000378:metabolism; D018417:Th1 Cells / Q000276:immunology; D018418:Th2 Cells / Q000276:immunology; D015854:Up-Regulation; D055815:Young Adult; D000098815:T-bet Transcription Factor
chemical_list: D017252:CD3 Complex; D054357:Chemokine CXCL10; D050990:GATA3 Transcription Factor; D020825:T-Box Domain Proteins; D000098815:T-bet Transcription Factor; D011070:Poly I-C