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Published 17 May 2004. doi:10.1084/jem.20032207
Rockefeller University Press, 0022-1007 $8.00
JEM, Volume 199, Number 10, 1379-1390
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Mannose-binding Lectin-deficient Mice Are Susceptible to Infection with Staphylococcus aureus

Lei Shi1, Kazue Takahashi1, Joseph Dundee1, Sarit Shahroor-Karni1, Steffen Thiel3, Jens Christian Jensenius3, Faten Gad2, Michael R. Hamblin2, Kedarnath N. Sastry1, and R. Alan B. Ezekowitz1

1 Laboratory of Developmental Immunology, Department of Pediatrics, and 2 Wellman Laboratory of Photomedicine, Department of Dermatology, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114
3 Department of Medical Microbiology and Immunology, University of Aarhus, DK-8000 Aarhus C, Denmark

Address correspondence to Kazue Takahashi, Laboratory of Developmental Immunology, Department of Pediatrics, Massachusetts General Hospital, Harvard Medical School, 55 Fruit Street, JRG 1402, Boston, MA 02114. Phone: (617) 726-1394; Fax: (617) 724-3248; email: ktakahashi1{at}partners.org

Gram-positive organisms like Staphylococcus aureus are a major cause of morbidity and mortality worldwide. Humoral response molecules together with phagocytes play a role in host responses to S. aureus. The mannose-binding lectin (MBL, also known as mannose-binding protein) is an oligomeric serum molecule that recognizes carbohydrates decorating a broad range of infectious agents including S. aureus. Circumstantial evidence in vitro and in vivo suggests that MBL plays a key role in first line host defense. We tested this contention directly in vivo by generating mice that were devoid of all MBL activity. We found that 100% of MBL-null mice died 48 h after exposure to an intravenous inoculation of S. aureus compared with 45% mortality in wild-type mice. Furthermore, we demonstrated that neutrophils and MBL are required to limit intraperitoneal infection with S. aureus. Our study provides direct evidence that MBL plays a key role in restricting the complications associated with S. aureus infection in mice and raises the idea that the MBL gene may act as a disease susceptibility gene against staphylococci infections in humans.

Key Words: mannose-binding lectin • MBL • infection • neutropenia • innate immunity

L. Shi and K. Takahashi contributed equally to this work.

Abbreviations used in this paper: CY, cyclophosphamide; LBP, lipopolysaccharide-binding protein; MASP, mannose-binding lectin–associated serine protease; MBL, mannose-binding lectin; rhMBL, recombinant human MBL.


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