ArticleClinical and experimental immunology2007
Low mannose-binding lectin complement activation function is associated with predisposition to Legionnaires' disease.
Article in Clinical and experimental immunology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
7 citing papers in PubMed, 21 citations in OpenAlex.
- The Influence of the Lectin Pathway of Complement Activation on Infections of the Respiratory System.Frontiers in immunology · 2020Review
- Severe community-acquired pneumonia.Critical care clinics · 2013Review
- The role of mannose-binding lectin in severe sepsis and septic shock.Mediators of inflammation · 2013Review
- No association between mannose-binding lectin deficiency and H1N1 2009 infection observed during the first season of this novel pandemic influenza virus.Human immunology · 2011Article
- Molecular pathogenesis of infections caused by Legionella pneumophila.Clinical microbiology reviews · 2010Review
- Mannose-binding lectin deficiency and respiratory tract infection.Journal of innate immunity · 2010Review
- Mannose-binding lectin serum levels are low in persons with clinically active coccidioidomycosis.Mycopathologia · 2009Article
Corrections and comments
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Authors and funding
6 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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.
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