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Related Experiment Videos

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

D P Eisen1, J Stubbs, D Spilsbury

  • 1Clinical Centre for Research Excellence in Infectious Diseases, Victorian Infectious Diseases Service, Royal Melbourne Hospital, Parkville, Victoria, Australia. damon.eisen@mh.org.au

Clinical and Experimental Immunology
|April 12, 2007
PubMed
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Mannose-binding lectin (MBL) functional deficiency, not MBL level, was linked to severe Legionnaires' disease in an Australian outbreak. This innate immune deficiency may increase susceptibility to Legionnaires' disease.

Area of Science:

  • Immunology
  • Infectious Diseases
  • Microbiology

Background:

  • Innate immune system deficiencies can lead to severe infections.
  • Legionnaires' disease is a severe infection that can be influenced by immune status.
  • Mannose-binding lectin (MBL) is a key component of the innate immune system.

Purpose of the Study:

  • To investigate the association between mannose-binding lectin (MBL) deficiency and Legionnaires' disease.
  • To determine if MBL deficiency played a role in the Melbourne Aquarium Legionnaires' disease outbreak.
  • To assess both MBL function and level in patients and controls.

Main Methods:

  • Serum samples from Legionnaires' disease patients and uninfected controls from the Melbourne Aquarium outbreak were analyzed.

Related Experiment Videos

  • Mannose-binding lectin (MBL) function was assessed by C4 deposition.
  • MBL level was measured by mannan-binding assay.

    • Main Results:

    • MBL function (C4 deposition) was significantly lower in Legionnaires' disease cases compared to controls.
    • A higher frequency of MBL deficiency (C4 deposition < 0.2 U/microl) was observed in cases, including those requiring hospitalization.
    • No significant difference in MBL mannan-binding levels was found between cases and controls.
    • MBL function and level remained stable in follow-up samples.

    Conclusions:

    • Functional deficiency in MBL-mediated complement activation is associated with an increased risk of developing Legionnaires' disease.
    • MBL deficiency may predispose individuals to severe infections like Legionnaires' disease.
    • The findings highlight the importance of MBL in innate immunity against bacterial pathogens such as Legionella.