| First Author | Takahashi K | Year | 2005 |
| Journal | Infect Immun | Volume | 73 |
| Issue | 12 | Pages | 8188-93 |
| PubMed ID | 16299314 | Mgi Jnum | J:104305 |
| Mgi Id | MGI:3611648 | Doi | 10.1128/IAI.73.12.8188-8193.2005 |
| Citation | Takahashi K, et al. (2005) Relative roles of complement factor 3 and mannose-binding lectin in host defense against infection. Infect Immun 73(12):8188-93 |
| abstractText | 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 x 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. |
