No Strong Relationship Between Components of the Lectin Pathway of Complement and Susceptibility to Pulmonary Tuberculosis.

Mycobacterium tuberculosis (TB) may utilise the lectin complement pathway to facilitate entry into its niche within macrophages. Previous studies examining mannose-binding lectin (MBL) in patients with TB have been limited by failure to correlate genotype/phenotype relationships. This study investigated serum levels and genotypes of MBL, Ficolin-2, Ficolin-3 and MASP-2 in 168 patients with pulmonary tuberculosis and 168 age/sex-matched controls. Low serum levels of MBL and Ficolin-2 were defined using cut-offs previously identified in the literature. Median MBL serum levels were higher in TB patients than controls-1400 ng/ml (IQR 435-2520) vs 1030 ng/ml (350-2050), p = 0.02-but this was not mirrored by a difference in MBL haplotype frequencies (MBL deficient haplotypes were observed in 11.9 % of TB patients and 11.3 % of controls). Severe Ficolin-2 deficiency (<1200 ng/ml) was more frequent in TB than controls (7.1 vs 3.0 %, odds ratio 2.51 95 % CI 0.86-7.28, p = 0.1) but the difference was not statistically significant. No relationship between Ficolin-2, Ficolin-3 or MASP-2 genotypes or serum levels and TB were observed. No strong relationship between the lectin complement pathway and pulmonary tuberculosis was observed. Previous data linking high MBL serum levels with TB were likely due to an acute phase response rather than a true effect on disease susceptibility.