title: Eotaxin-2 in sputum cell culture to evaluate asthma inflammation.
abstract: The aim of the present study was to elucidate whether the culture of cells recovered from induced sputum may represent a suitable model to evaluate cytokine and chemokine production by airway inflammatory cells. Sputum induction was performed in 21 normal subjects and 30 asthmatic patients. A total of 21 out of the 30 asthmatic patients were taking inhaled corticosteroids, while the remaining nine were steroid-naive asthmatics. The steroid-naive group was evaluated before and after a 14-day treatment with oral prednisone (40 mg.day(-1)). The supernatant of lysed and centrifuged sputum and the supernatant of sputum cell culture were analysed. Tumour necrosis factor-alpha, interleukin (IL)-8 (CXCL8), IL-1beta, IL-13 and eotaxin-2 (CCL24) concentrations were determined by specific ELISA. Eotaxin-2 production by cell culture was higher in the asthma group (131+/-108 pg.mL(-1)) than in the control group (36+/-41 pg.mL(-1)) and treatment with oral corticosteroids eliminated this difference. In addition, reduction of eotaxin-2 levels by corticosteroid treatment was greater in cell culture (81.3% reduction) than in sputum (26.4%). There was correlation between the decrease in eotaxin-2 production and the decrease in blood eosinophil number and between eotaxin-2 and eosinophils in sputum. Eotaxin-2 may play an important role in asthma and the response to corticosteroid treatment suggests that analysis of sputum cell culture is relevant as an inflammatory parameter.
authors.affiliation: Dept of Medicine, University of S. Paulo Medical School at Ribeirão Preto, Av. Bandeirantes 3900, Ribeirão Preto, Sãu Paulo, 14048-900, Brazil.
authors.forename: M E
authors.initials: ME
authors.lastname: Scheicher
authors.forename: M M
authors.initials: MM
authors.lastname: Teixeira
authors.forename: F Q
authors.initials: FQ
authors.lastname: Cunha
authors.forename: A L
authors.initials: AL
authors.lastname: Teixeira
authors.forename: J T
authors.initials: JT
authors.lastname: Filho
authors.forename: E O
authors.initials: EO
authors.lastname: Vianna
mesh_terms: D000280:Administration, Inhalation; D000284:Administration, Oral; D000328:Adult; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use; D001249:Asthma / Q000188:drug therapy / Q000276:immunology*; D019819:Budesonide / Q000627:therapeutic use; D002478:Cells, Cultured; D054423:Chemokine CCL24; D018925:Chemokines / Q000378:metabolism*; D019742:Chemokines, CC / Q000378:metabolism*; D016207:Cytokines / Q000378:metabolism*; D004797:Enzyme-Linked Immunosorbent Assay; D004804:Eosinophils / Q000187:drug effects / Q000276:immunology; D005260:Female; D005541:Forced Expiratory Volume / Q000187:drug effects / Q000502:physiology; D006801:Humans; D018793:Interleukin-13 / Q000378:metabolism; D053583:Interleukin-1beta / Q000378:metabolism; D016209:Interleukin-8 / Q000378:metabolism; D007958:Leukocyte Count; D008070:Lipopolysaccharides / Q000276:immunology; D008297:Male; D008875:Middle Aged; D011241:Prednisone / Q000627:therapeutic use; D012016:Reference Values; D012463:Saliva / Q000276:immunology*; D013223:Statistics as Topic; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D000893:Anti-Inflammatory Agents; C515484:CCL24 protein, human; D054423:Chemokine CCL24; D018925:Chemokines; D019742:Chemokines, CC; D016207:Cytokines; D018793:Interleukin-13; D053583:Interleukin-1beta; D016209:Interleukin-8; D008070:Lipopolysaccharides; D014409:Tumor Necrosis Factor-alpha; D019819:Budesonide; D011241:Prednisone