ArticleInfection and immunity2004
The alternative activation pathway and complement component C3 are critical for a protective immune response against Pseudomonas aeruginosa in a murine model of pneumonia.
Article in Infection and immunity, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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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
54 citing papers in PubMed, 104 citations in OpenAlex.
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- Novel broadly reactive monoclonal antibody protects againstInfection and immunity · 2025Article
- Fc-modification of anti-PcrV gene-encoded antibodies modulates complement-mediated killing of Pseudomonas aeruginosa.Frontiers in immunology · 2025Article
- The complement system: A key player in the host response to infections.European journal of immunology · 2024Review
- In Vivo Evolution of a Klebsiella pneumoniae Capsule Defect With wcaJ Mutation Promotes Complement-Mediated Opsonophagocytosis During Recurrent Infection.The Journal of infectious diseases · 2024Article
- The complement cascade in lung injury and disease.Respiratory research · 2024Review
- Factor H-related protein 1 promotes complement-mediated opsonization ofFrontiers in cellular and infection microbiology · 2024Article
- Complement activation drives the phagocytosis of necrotic cell debris and resolution of liver injury.Frontiers in immunology · 2024Article
- Systems serology in cystic fibrosis: Anti-Pseudomonas IgG1 responses and reduced lung function.Cell reports. Medicine · 2023Article
- Subversion of the Complement System by Pseudomonas aeruginosa.Journal of bacteriology · 2023Review
- Immunization with lytic polysaccharide monooxygenase CbpD induces protective immunity againstProceedings of the National Academy of Sciences of the United States of America · 2023Article
- Review
- Lung epithelial cell-derived C3 protects against pneumonia-induced lung injury.Science immunology · 2023Article
- Bitter taste signaling in tracheal epithelial brush cells elicits innate immune responses to bacterial infection.The Journal of clinical investigation · 2022Article
- Molecular Mechanisms Involved in Pseudomonas aeruginosa Bacteremia.Advances in experimental medicine and biology · 2022Review
- The lytic polysaccharide monooxygenase CbpD promotes Pseudomonas aeruginosa virulence in systemic infection.Nature communications · 2021Article
- Molecular Analysis of the Contribution of Alkaline Protease A and Elastase B to the Virulence ofFrontiers in cellular and infection microbiology · 2021Article
- Article
- Increased Alternative Complement Pathway Function and Improved Survival during Critical Illness.American journal of respiratory and critical care medicine · 2020Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Pseudomonas aeruginosa is a leading cause of hospital-acquired pneumonia, and approximately 80% of patients with cystic fibrosis are infected with this bacterium. To investigate the overall role of complement and the complement activation pathways in the host defense against P. aeruginosa pulmonary infection, we challenged C3-, C4-, and factor B-deficient mice with P. aeruginosa via intranasal inoculation. In these studies, C3(-/-) mice had a higher mortality rate than C3(+/+) mice. Factor B(-/-) mice, but not C4(-/-) mice, infected with P. aeruginosa had a mortality rate similar to that of C3(-/-) mice, indicating that in this model the alternative pathway of complement activation is required for the host defense against Pseudomonas infection. C3(-/-) mice had 6- to 7-fold more bacteria in the lungs and 48-fold more bacteria in the blood than did C3(+/+) mice at 24 h postinfection. In vitro, phagocytic cells from C3(+/+) or C3(-/-) mice exhibited a decreased ability to bind and/or ingest P. aeruginosa in the presence of C3-deficient serum compared to phagocytic cells in the presence of serum with sufficient C3. C3(-/-) mice displayed a significant increase in neutrophils in the lungs and had higher levels of interleukin-1beta (IL-1beta), IL-6, IL-10, KC, and MIP-2 in the lungs at 24 h postinfection than did C3(+/+) mice. Collectively, these results indicate that complement activation by the alternative pathway is critical for the survival of mice infected with P. aeruginosa and that the protection provided by complement is at least in part due to C3-mediated opsonization and phagocytosis of P. aeruginosa.
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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.