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Original Research: COMMUNITY-ACQUIRED PNEUMONIA |

Mannose-Binding Lectin Genotypes in Susceptibility to Community-Acquired Pneumonia

Henrik Endeman, MD; Bjorn L. Herpers, MD; Ben A. W. de Jong, BAS; G. Paul Voorn, MD, PhD; Jan C. Grutters, MD, PhD; Heleen van Velzen-Blad, MSc; Douwe H. Biesma, MD, PhD
Author and Funding Information

*From the Department of Intensive Care Medicine (Dr. Endeman), Onze Lieve Vrouwe Gasthuis, Amsterdam; Department of Internal Medicine (Dr. Biesma), University Medical Center Utrecht, Utrecht; and Departments of Pulmonary Medicine (Dr. Grutters) and Medical Microbiology and Immunology (Drs. Herpers and Voorn, Mr. de Jong, and Ms. van Velzen-Blad), St. Antonius Ziekenhuis Nieuwegein, Nieuwegein, the Netherlands.

Correspondence to: Henrik Endeman, MD, Department of Intensive Care, Diakonessenhuis, PO Box 80250, 3508TG, Utrect, the Netherlands; e-mail: henrik.endeman@planet.nl

Drs. Endeman and Herpers contributed equally to this article.


The authors have no financial or other potential conflicts of interest to disclose.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (www.chestjournal.org/misc/reprints.shtml).

For editorial comment see page 1112


Chest. 2008;134(6):1135-1140. doi:10.1378/chest.08-0642
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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.


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