Low mannose-binding lectin complement activation function is associated with predisposition to Legionnaires' disease.

Abstract

Innate immune system deficiency may predispose to severe infections such as Legionnaires' disease. We have investigated the role of mannose-binding lectin (MBL) deficiency in the Melbourne Aquarium Legionnaires' disease outbreak. Serum samples from patients and controls that were exposed but shown to be uninfected from the Melbourne Aquarium Legionnaires' disease outbreak were tested for MBL function (C4 deposition) and level (mannan-binding). MBL function was lower in Legionnaires' disease cases than in age- and sex-matched uninfected, exposed controls. The frequency of MBL deficiency with C4 deposition < 0.2 U/microl was significantly higher in Legionnaires' disease cases than in controls. This also applied to Legionnaires' disease cases requiring hospital care. There was no difference in MBL mannan-binding levels between Legionnaires' disease patients and controls. There was no significant interval change in MBL function or level after a mean of 46 days. MBL complement activation functional deficiency appears to predispose to Legionnaires' disease.

• Authors: D P Eisen, J Stubbs, D Spilsbury, J Carnie, J Leydon, B P Howden
• Journal: Clinical and experimental immunology (Clin Exp Immunol) Vol. 149 Issue 1 Pg. 97-102 (Jul 2007) ISSN: 0009-9104 [Print] England
• PMID: 17425652 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Complement C4
• Mannose-Binding Lectin

Topics

• Case-Control Studies
• Complement C4 (metabolism)
• Complement Pathway, Mannose-Binding Lectin (immunology)
• Disease Susceptibility
• Enzyme-Linked Immunosorbent Assay (methods)
• Female
• Humans
• Legionnaires' Disease (immunology)
• Male
• Mannose-Binding Lectin (deficiency, immunology)
• Prognosis
• Severity of Illness Index