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Sugar coating bronchiectasis
  1. Michael Loebinger
  1. Correspondence to Dr Michael Loebinger, Host Defence Unit, Division of Respiratory Medicine, Royal Brompton Hospital, London SW3 6NP, UK; M.Loebinger{at}rbht.nhs.uk

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Bronchiectasis is a condition characterised by damage and dilatation of airways. Clinically, this manifests with productive cough and recurrent infective exacerbations. The importance of bronchiectasis is increasingly becoming recognised with data demonstrating an increased prevalence and significant associated morbidity, mortality and healthcare burden.1 ,2 This has stimulated a surge in interest from academics and industry alike, with the start of several multicentre clinical trials. These have however been limited in part by the heterogeneity of bronchiectasis, with multiple different causes and significant variability in disease progression.3 The development of bronchiectasis severity scoring systems4 has helped to stratify patients into prognostic groups; however, the underlying basis for much of this heterogeneity has not been determined.

In Thorax, Taylor et al5 investigate one possible genetic predisposition to a worse bronchiectasis phenotype. They used the well-published, prospective cohort from the BLESS trial, which assessed the impact of long-term erythromycin on exacerbation rate.6 They focus their attention on the ability of the 112 patients to secrete histo-blood group antigens which is known to be a genetically determined autosomal trait encoded by the FUT2 gene.7 This gene encodes fucosyltransferases, which act to attach fucose to disaccharide precursors and hence control the expression of ABO antigens on the epithelial mucin glycans (‘secretors’). Approximately 25% of the population are known to be homozygous for nonsense mutations in the FUT2 gene which results in an inability to produce antigens on the epithelial surface and an absence of ABO antigens on secreted mucins, providing a different mucin glycan phenotype (‘non-secretors’).7 ,8 Microbes may use these carbohydrates for adherence, invasion, induction of virulence genes and as sources of carbon.8 Differences in such glycosylation between secretors and non-secretors may therefore impact the host–pathogen interaction, and previous studies have demonstrated that …

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