Mannose-binding lectin genotype and invasive pneumococcal infection

被引:35
作者
Moens, Leen
Van Hoeyveld, Erna
Peetermans, Willy E.
De Boeck, Christiane
Verhaegen, Jan
Bossuyt, Xavier
机构
[1] Univ Hosp Gasthuisberg, Expt Med Lab, CDG, B-3000 Louvain, Belgium
[2] Univ Hosp Gasthuisberg, Dept Lab Med, CDG, B-3000 Louvain, Belgium
[3] Univ Hosp Gasthuisberg, Dept Internal Med, CDG, B-3000 Louvain, Belgium
[4] Univ Hosp Gasthuisberg, Dept Pediat, CDG, B-3000 Louvain, Belgium
关键词
MBL; polymorphisms; invasive pneumococcal disease; Streptococcus pneumoniae;
D O I
10.1016/j.humimm.2006.04.014
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Invasive pneumococcal disease is a serious infection that primarily affects young children and elderly or immunocompromised persons, but it also can affect healthy persons. Mannose-binding lectin (MBL) is a mediator of innate host immunity that activates the complement pathway and directly opsonizes pathogens. Variant structural codon and promoter MBL alleles have been associated with susceptibility to infections. Sixty-three Belgian patients with invasive pneumococcal disease and 162 healthy Belgian controls were genotyped for MBL alleles. We found a nonsignificant increased risk between the MBL structural codon variants (52, 54, and 57) and invasive pneumococcal disease. Combining our data with similar data from Kronberg et al. (J Infect Dis 2002;185: 1517-20) indicated that MBL structural variants contributed to a small but significant increased risk of invasive pneumococcal disease. On the other hand, the -221 and -550 promoter allele distribution and the prevalence of the combined MBL structural and promoter -221 variant alleles were not significantly different between the patient group and the control group.
引用
收藏
页码:605 / 611
页数:7
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