Significantly increased levels of mannose‐binding lectin (MBL) in rheumatic heart disease: a beneficial role for MBL deficiency

• Published in: Clinical and experimental immunology Vol. 138; no. 3; pp. 521 - 525
• Main Authors: SCHAFRANSKI, M. D., STIER, A., NISIHARA, R., MESSIAS‐REASON, I. J. T.
• Format: Journal Article
• Language: English
• Published: Oxford, UK Blackwell Science Ltd 01.12.2004; Blackwell; Oxford University Press; Blackwell Science Inc
• Subjects: Adult; Aged; Biological and medical sciences; Clinical Studies; complement; Complement C3 - analysis; Complement C4 - analysis; Female; Fundamental and applied biological sciences. Psychology; Fundamental immunology; Humans; Immunopathology; Male; Mannose-Binding Lectin - blood; Mannose-Binding Lectin - deficiency; Mannose-Binding Lectin - immunology; mannose‐binding lectin; Medical sciences; Middle Aged; rheumatic fever; rheumatic heart disease; Rheumatic Heart Disease - blood; Rheumatic Heart Disease - immunology; Rheumatic Heart Disease - surgery; Immunopathology; Mannose binding lectin; Deficiency; Diseases of the osteoarticular system; Cardiovascular disease; Complement; mannose-binding lectin rheumatic heart disease complement rheumatic fever; Infection; Immunology; Streptococcal infection; Heart disease; Bacteriosis; Rheumatic fever
• ISSN: 0009-9104; 1365-2249
• DOI: 10.1111/j.1365-2249.2004.02645.x

SUMMARY Although mannose‐binding lectin (MBL) is known to be involved in the primary defense against microorganisms, there are emerging lines of evidence for an active proinflammatory role for MBL in different chronic diseases. In this study we determined the circulating levels of MBL in patients with rheumatic heart disease (RHD). A total of 100 patients (77 women, 23 men; mean age 45·8 ± 11 years, range 19–76 years) with chronic RHD, and a previous diagnosis of rheumatic fever, were studied. Transthoracic echocardiography was performed in all patients to evaluate valvular heart disease. Ninety‐nine healthy individuals matched for age, sex and ethnic origin were included as controls. MBL concentration was measured by enzyme‐linked immunosorbent assay and C3 and C4 levels by turbidimetry. MBL levels were significantly higher in patients with RHD than in healthy subjects (mean ± SEM: 3036·2 ± 298·9 ng/ml versus 1942·6 ± 185·5 ng/ml, P < 0·003). In addition, MBL deficiency was more prevalent in controls (17·1%) than in patients (9% P < 0·09). Concentrations of C4 were within the normal range (22·7 ± 0·8 mg/dl, normal: 10·0–40·0 mg/dl), while C3 concentrations were found to be elevated (109·2 ± 3·6 mg/dl, normal: 50·0–90·0 mg/dl). No correlation was observed between serum MBL levels and valve area or the type of surgical procedure. The significantly elevated circulating MBL levels in patients with RHD together with the greater prevalence of MBL deficiency in controls suggest that MBL may cause undesirable complement activation contributing to the pathogenesis of RHD.