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Mannose-binding lectin is present in the infected airway: a possible pulmonary defence mechanism
  1. Katy J Fidler (k.fidler{at}
  1. Institute of Child Health, United Kingdom
    1. Tom N Hilliard (tom.hilliard{at}
    1. Bristol Children's Hospital, United Kingdom
      1. Andy Bush (a.bush{at}
      1. Royal Brompton Hospital, United Kingdom
        1. Marina Johnson (m.johnson{at}
        1. Institute of child health, United Kingdom
          1. Eric Alton (e.alton{at}
          1. Imperial College, United Kingdom
            1. Duncan Geddes (d.geddes{at}
            1. Royal Brompton Hospital, United Kingdom
              1. Nigel Klein (n.klein{at}
              1. Institute of child health, United Kingdom
                1. Malcolm Turner (mwtedjim{at}
                1. Institute of child health, United Kingdom
                  1. Jane Davies (j.c.davies{at}
                  1. Royal Brompton Hospital, United Kingdom


                    Background: Mannose-binding lectin (MBL)-deficiency has been associated with infections of the respiratory tract and with increased disease severity in cystic fibrosis (CF). The mechanism is uncertain, and could relate either to systemic or local effects. The aim of this study was to determine, in a large human cohort, whether MBL is present on the airway surface in health or disease.

                    Methods: Children with and without respiratory infection (some with underlying disease) who had undergone bronchoalveolar lavage (BAL) had this fluid analysed for MBL and neutrophil elastase (NE). Levels were compared between groups; correlations were examined with inflammatory markers, both local and systemic, infective organisms and load.

                    Results: 85 children were recruited to the study. MBL was absent in the lavage of all 7 children without lung infection but present in 62% (8/13) of the children with acute pneumonia/pneumonitis, 23% (5/22) with recurrent respiratory tract infections, 17% (1/6) with primary ciliary dyskinesia and 8% (3/37) with CF (p<0.01). Children with acute pneumonia/pneumonitis had significantly (p<0.001) higher levels than those observed in the other groups. There was no relationship with organisms cultured or systemic markers of inflammation, although in the group with detectable BAL MBL, levels correlated positively (p=0.027) with levels of NE.

                    Conclusions: MBL is undetectable in the non infected airway but is present in a significant number of samples from those with lung infection. The levels demonstrated in BAL are of those which could be physiologically active and the protein may, therefore, be playing a role in host defence.

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