Mannose-binding lectin genotypes in susceptibility to community-acquired pneumonia.
BACKGROUND
Community-acquired pneumonia (CAP) is most frequently caused by Streptococcus pneumoniae, Haemophilus influenzae, atypical pathogens, and respiratory viruses. Susceptibility to CAP can be increased by single-nucleotide polymorphisms (SNPs) within the mannose-binding lectin (MBL) gene. We questioned whether MBL polymorphisms are associated with the susceptibility to and outcome of CAP and its most common pathogens.


METHODS
All adult patients presenting with CAP in a 23-month period were included in this study. Frequencies of SNPs were determined for the promoter X/Y and the three coding SNPs in exon 1 (A/0). Six genotypes were constructed representing patients with sufficient and deficient serum levels of MBL. The results of the patients with CAP were compared with control subjects.


RESULTS
In 199 patients and 223 control subjects, MBL genotypes were determined. There were no differences in MBL genotype frequencies between patients with CAP in general, pneumonia caused by S pneumoniae or H influenzae, and control subjects. The frequency of sufficient MBL genotypes was nonsignificantly higher in patients with pneumonia with Legionella sp and Mycoplasma pneumoniae. In Legionella spp, the sufficient YA/YA genotype was significantly more frequent than in control subjects (odds ratio [OR], 5.43; confidence interval [CI], 1.32 to 22.41; p = 0.02). The frequency of the MBL-deficient genotype was significantly higher in patients with viral (co)infections (OR, 2.36; CI, 1.06 to 5.26; p = 0.03) and nonsignificantly higher in patients with pneumococcal pneumonia and viral (co)infections. MBL genotypes had no effect on outcome.


CONCLUSIONS
MBL genotypes play a limited role in pneumococcal pneumonia. Sufficient MBL genotypes were more frequently found in a small group of patients with atypical pneumonia, and MBL-deficient genotypes were more frequently found in patients with viral (co)infections.
Endeman
Henrik
H
Department of Intensive Care Medicine, Onze Lieve Vrouwe Gasthuis, Amsterdam. Electronic address: henrik.endeman@planet.nl.
Herpers
Bjorn L
BL
Medical Microbiology and Immunology, St. Antonius Ziekenhuis Nieuwegein, Nieuwegein, the Netherlands.
de Jong
Ben A W
BAW
Medical Microbiology and Immunology, St. Antonius Ziekenhuis Nieuwegein, Nieuwegein, the Netherlands.
Voorn
G Paul
GP
Medical Microbiology and Immunology, St. Antonius Ziekenhuis Nieuwegein, Nieuwegein, the Netherlands.
Grutters
Jan C
JC
Departments of Pulmonary Medicine, St. Antonius Ziekenhuis Nieuwegein, Nieuwegein, the Netherlands.
van Velzen-Blad
Heleen
H
Medical Microbiology and Immunology, St. Antonius Ziekenhuis Nieuwegein, Nieuwegein, the Netherlands.
Biesma
Douwe H
DH
Department of Internal Medicine, University Medical Center Utrecht, Utrecht.
D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D016022:Case-Control Studies; D015331:Cohort Studies; D017714:Community-Acquired Infections / Q000235:genetics / Q000382:microbiology / Q000401:mortality; D005260:Female; D020022:Genetic Predisposition to Disease; D006801:Humans; D008297:Male; D037601:Mannose-Binding Lectin / Q000235:genetics*; D008875:Middle Aged; D018410:Pneumonia, Bacterial / Q000235:genetics* / Q000382:microbiology / Q000401:mortality; D011024:Pneumonia, Viral / Q000235:genetics* / Q000401:mortality / Q000821:virology; D020641:Polymorphism, Single Nucleotide / Q000235:genetics*; D016896:Treatment Outcome
C445619:MBL2 protein, human; D037601:Mannose-Binding Lectin