ArticleInfection and immunity2005
Relative roles of complement factor 3 and mannose-binding lectin in host defense against infection.
Article in Infection and immunity, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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
18 citing papers in PubMed, 34 citations in OpenAlex.
- Do microenvironmental changes in degenerative disc disease reflect in systemic circulation? A proteomic investigation.Clinical proteomics · 2025Article
- Dynamic alterations and clinical implications of the plasma proteome in pediatric sepsis.European journal of medical research · 2025Article
- Cellular uptake and in vivo distribution of mesenchymal-stem-cell-derived extracellular vesicles are protein corona dependent.Nature nanotechnology · 2024Article
- Reg4 and complement factor D prevent the overgrowth of E. coli in the mouse gut.Communications biology · 2020Article
- Low circulating mannan-binding lectin levels correlate with increased frequency and severity of febrile episodes in myeloma patients who undergo ASCT and do not receive antibiotic prophylaxis.Bone marrow transplantation · 2017Article
- Mannose-binding lectin and l-ficolin polymorphisms in patients with community-acquired pneumonia caused by intracellular pathogens.Immunology · 2017Article
- Deficiency of the Complement Component 3 but Not Factor B Aggravates Staphylococcus aureus Septic Arthritis in Mice.Infection and immunity · 2016Article
- Association of mannose-binding lectin 2 gene polymorphisms with persistent Staphylococcus aureus bacteremia.PloS one · 2014Article
- CD137 expressed on neutrophils plays dual roles in antibacterial responses against Gram-positive and Gram-negative bacterial infections.Infection and immunity · 2013Article
- Mannose-binding lectin regulates host resistance and pathology during experimental infection with Trypanosoma cruzi.PloS one · 2012Article
- Staphylococcus aureus virulence is enhanced by secreted factors that block innate immune defenses.Journal of innate immunity · 2012Article
- Mannose-binding lectin and the balance between immune protection and complication.Expert review of anti-infective therapy · 2011Review
- Distinct different contributions of the alternative and classical complement activation pathway for the innate host response during sepsis.Journal of immunology (Baltimore, Md. : 1950) · 2011Article
- Deficiency of mannose-binding lectin greatly increases antibody response in a mouse model of vaccination.Clinical immunology (Orlando, Fla.) · 2009Article
- Bridging effect of recombinant human mannose-binding lectin in macrophage phagocytosis of Escherichia coli.Immunology · 2008Article
- Mannose-binding lectin haplotypes influence Brucella abortus infection in the water buffalo (Bubalus bubalis).Immunogenetics · 2008Article
- Mannose-binding lectin enhances Toll-like receptors 2 and 6 signaling from the phagosome.The Journal of experimental medicine · 2008Article
- Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
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 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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.