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Pulmonary Medicine
Volume 2012, Article ID 469128, 6 pages
Research Article

Mannose-Binding Lectin Promoter Polymorphisms and Gene Variants in Pulmonary Tuberculosis Patients from Cantabria (Northern Spain)

1Servicio de Inmunología, Hospital Universitario Marqués de Valdecilla, Avenida de Valdecilla s/n, 39008 Santander, Spain
2Unidad de Enfermedades Infecciosas, Departamento de Medicina Interna, Hospital Universitario Marqués de Valdecilla, Universidad de Cantabria, 39011 Santander, Spain

Received 25 September 2012; Revised 16 November 2012; Accepted 18 November 2012

Academic Editor: José R. Lapa e Silva

Copyright © 2012 J.-Gonzalo Ocejo-Vinyals et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Mannose-binding lectin is a central molecule of the innate immune system. Mannose-binding lectin 2 promoter polymorphisms and structural variants have been associated with susceptibility to tuberculosis. However, contradictory results among different populations have been reported, resulting in no convincing evidence of association between mannose-binding lectin 2 and susceptibility to tuberculosis. For this reason, we conducted a study in a well genetically conserved Spanish population in order to shed light on this controversial association. We analysed the six promoter and structural mannose-binding lectin 2 gene variants in 107 patients with pulmonary tuberculosis and 441 healthy controls. Only D variant and HYPD haplotype were significantly more frequents in controls which would indicate that this allele could confer protection against pulmonary tuberculosis, but this difference disappeared after statistical correction. Neither the rest of alleles nor the haplotypes were significantly associated with the disease. These results would indicate that mannose-binding lectin promoter polymorphisms and gene variants would not be associated with an increased risk to pulmonary tuberculosis. Despite the slight trend of the D allele and HYPD haplotype in conferring protection against pulmonary tuberculosis, susceptibility to this disease would probably be due to other genetic factors, at least in our population.