No strong relationship between components of the lectin pathway of complement and susceptibility to pulmonary tuberculosis

James D. Chalmers (Lead / Corresponding author), Misao Matsushita, David C. Kilpatrick, Adam T. Hill

    Research output: Contribution to journalArticle

    10 Citations (Scopus)

    Abstract

    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.

    Original languageEnglish
    Pages (from-to)1731-1737
    Number of pages7
    JournalInflammation
    Volume38
    Issue number4
    Early online date12 Mar 2015
    DOIs
    Publication statusPublished - Aug 2015

    Fingerprint

    Mannose-Binding Lectin Complement Pathway
    Mannose-Binding Lectin
    Pulmonary Tuberculosis
    Tuberculosis
    Mannose-Binding Protein-Associated Serine Proteases
    Serum
    Genotype
    Haplotypes
    Acute-Phase Reaction
    Disease Susceptibility
    Mycobacterium tuberculosis
    ficolin
    Macrophages
    Odds Ratio
    Phenotype

    Cite this

    Chalmers, James D. ; Matsushita, Misao ; Kilpatrick, David C. ; Hill, Adam T. / No strong relationship between components of the lectin pathway of complement and susceptibility to pulmonary tuberculosis. In: Inflammation. 2015 ; Vol. 38, No. 4. pp. 1731-1737.
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    abstract = "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.",
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    No strong relationship between components of the lectin pathway of complement and susceptibility to pulmonary tuberculosis. / Chalmers, James D. (Lead / Corresponding author); Matsushita, Misao; Kilpatrick, David C.; Hill, Adam T.

    In: Inflammation, Vol. 38, No. 4, 08.2015, p. 1731-1737.

    Research output: Contribution to journalArticle

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