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  • Original Article
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Mannose-binding lectin gene polymorphism predicts hospital admissions for COPD infections

Abstract

Infection frequently causes exacerbations of chronic obstructive pulmonary disease (COPD). Mannose-binding lectin (MBL) is a pattern-recognition receptor that assists in clearing microorganisms. Polymorphisms in the MBL2 gene reduce serum MBL levels and are associated with risk of infection. We studied whether the MBL2 codon 54 B allele affected serum MBL levels, admissions for infective exacerbation in COPD and disease susceptibility. Polymorphism frequency was determined by PCR-RFLP in 200 COPD patients and 104 smokers with normal lung function. Serum MBL was measured as mannan-binding activity in a subgroup of 82 stable COPD patients. Frequency of COPD admissions for infective exacerbation was ascertained for a 2-year period. The MBL2 codon 54 B allele reduced serum MBL in COPD patients. In keeping, patients carrying the low MBL-producing B allele had increased risk of admission for infective exacerbation (OR 4.9, Pcorrected=0.011). No association of MBL2 genotype with susceptibility to COPD was detected. In COPD, serum MBL is regulated by polymorphism at codon 54 in its encoding gene. Low MBL-producing genotypes were associated with more frequent admissions to hospital with respiratory infection, suggesting that the MBL2 gene is disease-modifying in COPD. MBL2 genotype should be explored prospectively as a prognostic marker for infection risk in COPD.

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Acknowledgements

We sincerely thank the patients and staff of The Prince Charles Hospital, the Respiratory Investigations Unit and Phlebotomy. This work was supported by The Prince Charles Hospital Foundation, an NHMRC Postgraduate Medical Scholarship (for IAY) and an NHMRC Project Grant No. 970283 (to EMA). Statistical advice was supported by an ARC SPIRT Grant No. C10024120.

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Correspondence to I A Yang.

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Yang, I., Seeney, S., Wolter, J. et al. Mannose-binding lectin gene polymorphism predicts hospital admissions for COPD infections. Genes Immun 4, 269–274 (2003). https://doi.org/10.1038/sj.gene.6363961

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