title: Inflammatory cell populations and cytokine mRNA expression in the nasal mucosa in aspirin-sensitive rhinitis.
abstract: Aspirin-sensitive rhinitis is characterized by severe perennial nasal congestion and discharge. The study questioned whether this disease, like immunoglobulin E-mediated rhinitis, might be associated with local recruitment and activation of T-lymphocytes, mast cells and eosinophils with parallel increases in "T-helper2-type" cytokines. Nasal biopsies from 10 patients with aspirin-sensitive rhinitis and 12 healthy controls subjects were studied. Nasal mucosal sections were examined by immunohistochemistry in order to determine cell phenotypes and by in situ hybridization to detect cells expressing messenger ribonucleic acid (mRNA) for cytokines. In aspirin-sensitive rhinitis there were increases in total (CD3+) (p=0.05) and activated (CD25+) T-cells (p=0.007), total (major basic protein (MBP) positive) (p=0.004) and activated (monoclonal antibody which recognizes the cleaved form of eosinophil cationic protein (EG2) positive) eosinophils (p=0.003), tryptase+ mast cells (p=0.04) and CD68+ macrophages (p=0.002). Neutrophils and cells expressing human leukocyte antigen-DR were no different. Marked increases were observed in the numbers of interleukin (IL)-5 mRNA+ cells (p=0.004) in aspirin-sensitive patients, whereas lower numbers of IL-4 mRNA+ cells were observed, with a trend for a difference from controls (p=0.07). No differences were observed for either IL-2 or interferon-gamma. In conclusion, in aspirin-sensitive rhinitis there is intense inflammation of the nasal mucosa characterised by T-lymphocytes, eosinophils and mast cells. The predominance of macrophages and disproportionate increase in interleukin-5 compared to interleukin-4 messenger ribonucleic acid expression suggests that factors other than "allergic" mechanisms may be important in this disease.
authors.affiliation: Upper Respiratory Medicine, Imperial College School of Medicine at the National Heart and Lung Institute, London, UK.
authors.forename: E M
authors.initials: EM
authors.lastname: Varga
authors.forename: M R
authors.initials: MR
authors.lastname: Jacobson
authors.forename: K
authors.initials: K
authors.lastname: Masuyama
authors.forename: S
authors.initials: S
authors.lastname: Rak
authors.forename: S J
authors.initials: SJ
authors.lastname: Till
authors.forename: Y
authors.initials: Y
authors.lastname: Darby
authors.forename: Q
authors.initials: Q
authors.lastname: Hamid
authors.forename: V
authors.initials: V
authors.lastname: Lund
authors.forename: G K
authors.initials: GK
authors.lastname: Scadding
authors.forename: S R
authors.initials: SR
authors.lastname: Durham
mesh_terms: D000328:Adult; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000009:adverse effects*; D015703:Antigens, CD / Q000378:metabolism; D001241:Aspirin / Q000009:adverse effects*; D001706:Biopsy; D001798:Blood Proteins / Q000378:metabolism; D053818:Chymases; D047091:Eosinophil Granule Proteins; D005260:Female; D006801:Humans; D016130:Immunophenotyping; D017403:In Situ Hybridization; D007378:Interleukins / Q000096:biosynthesis / Q000235:genetics*; D007962:Leukocytes / Q000378:metabolism / Q000473:pathology*; D008264:Macrophages / Q000378:metabolism / Q000473:pathology; D008297:Male; D008407:Mast Cells / Q000378:metabolism / Q000473:pathology*; D008875:Middle Aged; D009297:Nasal Mucosa / Q000187:drug effects / Q000378:metabolism / Q000473:pathology*; D012333:RNA, Messenger / Q000378:metabolism*; D012221:Rhinitis, Allergic, Perennial / Q000139:chemically induced / Q000378:metabolism / Q000473:pathology*; D012260:Ribonucleases; D012697:Serine Endopeptidases / Q000378:metabolism; D053802:Tryptases
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D015703:Antigens, CD; D001798:Blood Proteins; D047091:Eosinophil Granule Proteins; D007378:Interleukins; D012333:RNA, Messenger; D012260:Ribonucleases; D012697:Serine Endopeptidases; C083294:chymase 2; D053818:Chymases; D053802:Tryptases; D001241:Aspirin