title: Indirect evidence of nasal inflammation assessed by titration of inflammatory mediators and enumeration of cells in nasal secretions of patients with chronic rhinitis.
abstract: Pathophysiologic mechanisms of perennial rhinitis are poorly understood. The characterization of inflammation was studied in nasal lavage of patients with perennial rhinitis by the enumeration of cells involved in the allergic inflammation and the measurement of six mediators released in nasal secretions to determine whether some mediators were relevant for the etiologic diagnosis and the occurrence of symptoms. Ten healthy subjects and 57 patients with perennial rhinitis were placed into four groups according to the symptoms they presented at the time of the study and the origin of the allergy. Allergy was characterized by the history, skin prick tests to standardized allergens, and RAST. Eosinophil protein X (EPX), tryptase, histamine, myeloperoxidase, prostaglandin D2, and leukotriene C4/D4 (LTC4/D4) were measured in nasal lavage by enzyme assay or radioimmunoassay. Eosinophils and neutrophils were enumerated after cytocentrifugation of the lavage fluid and May Grunwald Giemsa staining. Tryptase, myeloperoxidase and EPX but not histamine levels were increased in all four patient groups. Eosinophils, LTC4/D4, and prostaglandin D2 were significantly (p < 0.001, p < 0.03, and p < 0.01) increased in allergic and symptomatic patients. EPX was significantly increased in symptomatic allergic and nonallergic patients. This study suggests the involvement of mast cells, neutrophils, and eosinophils, but the latter cells appear to have a more prominent role. The importance of EPX and LTC4/D4 in the characterization of chronic symptomatic rhinitis was also observed.
authors.affiliation: Clinique des Maladies Respiratoires, Hopital l'Aiguelongue, Centre Hospitalier Universitaire, Montpellier, France.
authors.forename: J
authors.initials: J
authors.lastname: Knani
authors.forename: A
authors.initials: A
authors.lastname: Campbell
authors.forename: I
authors.initials: I
authors.lastname: Enander
authors.forename: C G
authors.initials: CG
authors.lastname: Peterson
authors.forename: F B
authors.initials: FB
authors.lastname: Michel
authors.forename: J
authors.initials: J
authors.lastname: Bousquet
mesh_terms: D000293:Adolescent; D000328:Adult; D001798:Blood Proteins / Q000032:analysis / Q000494:pharmacology; D053818:Chymases; D047091:Eosinophil Granule Proteins; D005260:Female; D006632:Histamine / Q000032:analysis / Q000494:pharmacology; D006801:Humans; D015289:Leukotrienes / Q000032:analysis / Q000494:pharmacology; D008297:Male; D008407:Mast Cells / Q000166:cytology; D008875:Middle Aged; D009297:Nasal Mucosa / Q000737:chemistry / Q000166:cytology / Q000378:metabolism*; D009195:Peroxidase / Q000032:analysis / Q000494:pharmacology; D015230:Prostaglandin D2 / Q000032:analysis / Q000494:pharmacology; D012220:Rhinitis / Q000503:physiopathology*; D012221:Rhinitis, Allergic, Perennial / Q000473:pathology; D012260:Ribonucleases; D012697:Serine Endopeptidases / Q000032:analysis / Q000494:pharmacology; D007507:Therapeutic Irrigation; D053802:Tryptases
chemical_list: D001798:Blood Proteins; D047091:Eosinophil Granule Proteins; D015289:Leukotrienes; D006632:Histamine; D009195:Peroxidase; D012260:Ribonucleases; D012697:Serine Endopeptidases; C083294:chymase 2; D053818:Chymases; D053802:Tryptases; D015230:Prostaglandin D2