title: Inflammatory response in induced sputum mononuclear cells from patients with acute exacerbation of asthma.
abstract: Examination of sputum provides a direct method to investigate airway inflammation non-invasively in particular Th1 (IL-2, IFN-gamma) and Th2 (IL-4, IL-10) cytokine production. IL-2, IL-4, IL-10 and IFN-gamma cytokine were studied in induced sputum mononuclear cells of asthmatic patients. Sputum induction was performed on 10 patients and 10 normal controls. Basal and mitogen-stimulated cytokine production was determined in induced sputum T-cell culture. Supernatants were collected and assayed not only with specific ELISA but also with polymerase chain reaction (PCR) techniques. Data showed a significantly higher production of IL-10 by both the ELISA and the RT-PCR techniques in asthmatic patients compared with sputum mononuclear cells from healthy controls. IL-4 production was detected at a low level using the ELISA method in asthmatic patients. The RT-PCR analysis detected a significantly IL-4-mRNA expression in all asthmatic patients, compared with controls. Results of IL-10 and IL-4 mRNA expression were reproducible. We did not find any alteration in the expression of the type 1 derived cytokines (IL-2 and IFN-gamma) in asthmatic patients or in healthy controls. Our study showed a tendency of induced sputum mononuclear cells to express a Th2-like cytokine pattern in acute exacerbation of asthmatic patients, where IL-10 and IL-4 are synthesized in larger amounts. The combination of sputum induction as a non-invasive tool to explore the lung and the identification of disease-associated cytokine expression and of specific cytokine mRNA should help elucidate mechanisms of the immunologically mediated inflammatory responses in asthma.
authors.affiliation: A. Mami Hospital, Department of Pediatric Respiratory Diseases, Ariana. Kamel.Hamzaoui@fmt.rnu.tn
authors.forename: A
authors.initials: A
authors.lastname: Hamzaoui
authors.forename: M B
authors.initials: MB
authors.lastname: Brahim
authors.forename: A
authors.initials: A
authors.lastname: Zhioua
authors.forename: K
authors.initials: K
authors.lastname: Ayed
authors.forename: K
authors.initials: K
authors.lastname: Hamzaoui
mesh_terms: D000328:Adult; D001249:Asthma / Q000235:genetics / Q000276:immunology* / Q000473:pathology*; D001483:Base Sequence; D016022:Case-Control Studies; D016207:Cytokines / Q000096:biosynthesis / Q000235:genetics; D017931:DNA Primers / Q000235:genetics; D004797:Enzyme-Linked Immunosorbent Assay; D006801:Humans; D018836:Inflammation Mediators / Q000378:metabolism*; D007371:Interferon-gamma / Q000096:biosynthesis / Q000235:genetics; D016753:Interleukin-10 / Q000096:biosynthesis / Q000235:genetics; D007376:Interleukin-2 / Q000096:biosynthesis / Q000235:genetics; D015847:Interleukin-4 / Q000096:biosynthesis / Q000235:genetics; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013183:Sputum / Q000166:cytology* / Q000276:immunology*; D018417:Th1 Cells / Q000276:immunology / Q000473:pathology; D018418:Th2 Cells / Q000276:immunology / Q000473:pathology
chemical_list: D016207:Cytokines; D017931:DNA Primers; D018836:Inflammation Mediators; D007376:Interleukin-2; D012333:RNA, Messenger; D016753:Interleukin-10; D015847:Interleukin-4; D007371:Interferon-gamma