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

Damon P Eisen, J Stubbs, D Spilsbury, John Carnie, J Leydon, Benjamin Peter Howden

Research output: Contribution to journalArticleResearchpeer-review

18 Citations (Scopus)

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.
Original languageEnglish
Pages (from-to)97 - 102
Number of pages6
JournalClinical and Experimental Immunology
Volume149
Issue number1
DOIs
Publication statusPublished - 2007

Cite this