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Rhinovirus exposure impairs immune responses to bacterial products in human alveolar macrophages
  1. Brian G Oliver (boliver{at}
  1. The Univeristy of Sydney, Australia
    1. Sam Lim (sam.x.lim{at}
    1. ANZAC research institute, Univeristy of Sydney, Australia
      1. Peter Wark (peter.wark{at}
      1. Respiratory Medicine HMRI, Australia
        1. Vasile Laza-Stanca (vasile.laza-stanca{at}
        1. Department of Respiratory Medicine, Imperial College, United Kingdom
          1. Nicholas J.C. King (nickk{at}
          1. The University of Sydney, Australia
            1. Judith L Black (judblack{at}
            1. University of Sydney Department of Pharmacology, Australia
              1. Janette K Burgess (janette{at}
              1. University of Sydney Department of Pharmacology, Australia
                1. Michael Roth (michaelr{at}
                1. The Woolcock Institute for Medical Research, Australia
                  1. Sebastian L Johnston (s.johnston{at}
                  1. Department of Respiratory Medicine, National Heart and Lung Institute, Imperial College London,, United Kingdom


                    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. Therefore we investigated whether rhinovirus modifies cytokine release, the pattern recognition receptor (PRR) expression and phagocytosis by human alveolar macrophages in response to bacterial products. Viable rhinovirus was detected in macrophages up to 3 days after exposure and viral RNA expression persisted to 10 days. Infectious but not UV-inactivated rhinovirus increased TNF-α and IL-8 release by macrophages. In contrast, infectious rhinovirus impaired lipopolysaccharide and lipoteichoic acid induced TNF-α and IL-8 secretion by macrophages. Rhinovirus-induced impairment of macrophage antibacterial immune responses did not involve IL-10, PGE2, or down-regulation of TLR2. Furthermore the macrophage phagocytic response to labelled bacterial particles, but not to latex beads, was impaired. In conclusion, we 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.

                    • COPD
                    • Rhinovirus
                    • asthma
                    • bacteria
                    • superinfection

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