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• W2155393695 abstract "ABSTRACT Staphylococcus aureus is a major cause of severe nosocomial and community-acquired infections. Phagocytes and humoral molecules, including complement, have been proposed to cooperate in host defense against gram-positive bacteria. Circumstantial evidence indicates a role for complement, but this has not been formally defined. Complement activation is initiated by the classical, alternative, or lectin pathway, with the latter requiring mannose-binding lectin (MBL, also known as mannose-binding protein). MBL is an oligomeric serum protein that recognizes carbohydrates decorating a broad range of infectious agents, including S. aureus . We previously reported that MBL null mice were highly susceptible to S. aureus infection, confirming that MBL plays a key role in first-line host defense. In this study, we evaluated the relative roles of C3 and MBL against S. aureus infection by generating MBL × C3 null mice to compare with C3 single null mice. C3 deficiency alone significantly reduced survival to 19% from 97% of wild-type mice ( P < 0.0001). Surprisingly, an additional MBL deficiency reduced the survival further to 7% ( P < 0.0001). However, the MBL deficiency alone had a smaller though significant effect on survival, which was 77% ( P = 0.018 versus wild-type mice). These results confirm an essential function for complement in host resistance against S. aureus infection but also identify an MBL-dependent mechanism that is C3 independent." @default.
• W2155393695 created "2016-06-24" @default.
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• W2155393695 date "2005-12-01" @default.
• W2155393695 modified "2023-09-27" @default.
• W2155393695 title "Relative Roles of Complement Factor 3 and Mannose-Binding Lectin in Host Defense against Infection" @default.
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• W2155393695 doi "https://doi.org/10.1128/iai.73.12.8188-8193.2005" @default.
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