title: Rhinovirus exposure impairs immune responses to bacterial products in human alveolar macrophages.
abstract: BACKGROUND
  Rhinovirus infection is responsible for considerable morbidity and mortality as the major cause of exacerbations of asthma, and is also known to induce exacerbations of cystic fibrosis and chronic obstructive pulmonary disease. Exacerbations of these diseases are also frequently associated with bacterial and atypical bacterial infection. Alveolar macrophages are the major immune cells in the airways and are important in defence against bacterial infections.
  
  
  METHODS
  The authors investigated whether rhinovirus modifies cytokine release, the pattern recognition receptor expression and phagocytosis by human alveolar macrophages in response to bacterial products.
  
  
  RESULTS
  Viable rhinovirus was detected in macrophages up to 3 days after exposure and viral RNA expression persisted for 10 days. Infectious but not UV inactivated rhinovirus increased tumour necrosis factor alpha (TNFalpha) and interleukin (IL)8 release by macrophages. In contrast, infectious rhinovirus impaired lipopolysaccharide and lipoteichoic acid induced TNFalpha and IL8 secretion by macrophages. Rhinovirus induced impairment of macrophage antibacterial immune responses did not involve IL10, prostaglandin E(2) or downregulation of Toll-like receptor 2. Furthermore, the macrophage phagocytic response to labelled bacterial particles, but not to latex beads, was impaired.
  
  
  CONCLUSIONS
  The authors have identified impairment of cytokine responses to bacterial lipopolysaccharide and lipoteichoic acid by alveolar macrophages in response to infectious rhinovirus. Virus induced impairment of antibacterial host defence has important implications in the pathogenesis of exacerbations of respiratory diseases.
authors.affiliation: Discipline of Pharmacology, The University of Sydney, Sydney, NSW 2006, Australia. boliver@med.usyd.edu.au
authors.forename: B G G
authors.initials: BG
authors.lastname: Oliver
authors.forename: S
authors.initials: S
authors.lastname: Lim
authors.forename: P
authors.initials: P
authors.lastname: Wark
authors.forename: V
authors.initials: V
authors.lastname: Laza-Stanca
authors.forename: N
authors.initials: N
authors.lastname: King
authors.forename: J L
authors.initials: JL
authors.lastname: Black
authors.forename: J K
authors.initials: JK
authors.lastname: Burgess
authors.forename: M
authors.initials: M
authors.lastname: Roth
authors.forename: S L
authors.initials: SL
authors.lastname: Johnston
mesh_terms: D015536:Down-Regulation; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D006090:Gram-Negative Bacteria / Q000276:immunology; D016905:Gram-Negative Bacterial Infections / Q000276:immunology; D006094:Gram-Positive Bacteria / Q000276:immunology; D016908:Gram-Positive Bacterial Infections / Q000276:immunology; D006801:Humans; D007111:Immunity, Cellular; D016209:Interleukin-8 / Q000378:metabolism; D008070:Lipopolysaccharides / Q000494:pharmacology; D016676:Macrophages, Alveolar / Q000276:immunology* / Q000821:virology; D008297:Male; D008875:Middle Aged; D010587:Phagocytosis / Q000276:immunology; D010850:Picornaviridae Infections / Q000276:immunology* / Q000821:virology; D012229:Rhinovirus / Q000276:immunology*; D013682:Teichoic Acids / Q000494:pharmacology; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D016209:Interleukin-8; D008070:Lipopolysaccharides; D013682:Teichoic Acids; D014409:Tumor Necrosis Factor-alpha; C009900:lipoteichoic acid