Increased proinflammatory responses from asthmatic human airway smooth muscle cells in response to rhinovirus infection

• Published in: Respiratory research 2006-05, Vol.7 (1), p.71-71, Article 71
• Main Authors: Oliver, Brian G G, Johnston, Sebastian L, Baraket, Melissa, Burgess, Janette K, King, Nicholas J C, Roth, Michael, Lim, Sam, Black, Judith L
• Format: Article
• Language: English
• Subjects: Adolescent; Adult; Asthma; Asthma - immunology; Asthma - virology; B cells; CCAAT-Enhancer-Binding Protein-alpha - immunology; Cell Death; Cells, Cultured; Comparative analysis; Cytokines; Enzyme-linked immunosorbent assay; Female; Humans; Infection; Intercellular Adhesion Molecule-1 - biosynthesis; Intercellular Adhesion Molecule-1 - immunology; Interleukin-6 - biosynthesis; Interleukin-6 - genetics; Interleukin-6 - immunology; Interleukin-8 - biosynthesis; Male; Myocytes, Smooth Muscle - immunology; Myocytes, Smooth Muscle - virology; Respiratory System - virology; Rhinovirus; Rhinovirus - immunology; Rhinovirus - pathogenicity; Smooth muscle; Transcription, Genetic - immunology; Transfection
• ISSN: 1465-993X; 1465-9921; 1465-993X; 1465-9921
• DOI: 10.1186/1465-9921-7-71

Exacerbations of asthma are associated with viral respiratory tract infections, of which rhinoviruses (RV) are the predominant virus type. Airway smooth muscle is important in asthma pathogenesis, however little is known about the potential interaction of RV and human airway smooth muscle cells (HASM). We hypothesised that rhinovirus induction of inflammatory cytokine release from airway smooth muscle is augmented and differentially regulated in asthmatic compared to normal HASM cells. HASM cells, isolated from either asthmatic or non-asthmatic subjects, were infected with rhinovirus. Cytokine production was assayed by ELISA, ICAM-1 cell surface expression was assessed by FACS, and the transcription regulation of IL-6 was measured by luciferase activity. RV-induced IL-6 release was significantly greater in HASM cells derived from asthmatic subjects compared to non-asthmatic subjects. This response was RV specific, as 5% serum- induced IL-6 release was not different in the two cell types. Whilst serum stimulated IL-8 production in cells from both subject groups, RV induced IL-8 production in only asthmatic derived HASM cells. The transcriptional induction of IL-6 was differentially regulated via C/EBP in the asthmatic and NF-kappaB + AP-1 in the non-asthmatic HASM cells. This study demonstrates augmentation and differential transcriptional regulation of RV specific innate immune response in HASM cells derived from asthmatic and non-asthmatics, and may give valuable insight into the mechanisms of RV-induced asthma exacerbations.