ArticleJournal of immunology (Baltimore, Md. : 1950)2013
Complement factor B is the downstream effector of TLRs and plays an important role in a mouse model of severe sepsis.
Article in Journal of immunology (Baltimore, Md. : 1950), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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Who cites it
52 citing papers in PubMed, 79 citations in OpenAlex.
- Redundant and distinct mechanisms suppress innate immune activation during SARS-CoV-2 infection.PLoS biology · 2026Article
- The role of the complement system in gastrointestinal-related diseases.Frontiers in immunology · 2026Review
- Urine Complement Factor Ba Identifies Persistent Acute Kidney Injury and Organ Failures in Critically Ill Adults.Kidney international reports · 2025Article
- Article
- Comprehensive time-course gene expression evaluation of high-risk beef cattle to establish immunological characteristics associated with undifferentiated bovine respiratory disease.Frontiers in immunology · 2024Article
- Extracellular RNA Sensing Mediates Inflammation and Organ Injury in a Murine Model of Polytrauma.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- The complement system in pediatric acute kidney injury.Pediatric nephrology (Berlin, Germany) · 2023Review
- Lung epithelial cell-derived C3 protects against pneumonia-induced lung injury.Science immunology · 2023Article
- Characterization of a proteomic profile associated with organ dysfunction and mortality of sepsis and septic shock.PloS one · 2022Article
- Complement as driver of systemic inflammation and organ failure in trauma, burn, and sepsis.Seminars in immunopathology · 2021Review
- Targeting Toll-Like Receptors in Sepsis: From Bench to Clinical Trials.Antioxidants & redox signaling · 2021Review
- The human type 2 diabetes-specific visceral adipose tissue proteome and transcriptome in obesity.Scientific reports · 2021Article
- PMMA-Based Continuous Hemofiltration Modulated Complement Activation and Renal Dysfunction in LPS-Induced Acute Kidney Injury.Frontiers in immunology · 2021Article
- Antioxidative, Antiapoptotic, and Anti-Inflammatory Effects of Apamin in a Murine Model of Lipopolysaccharide-Induced Acute Kidney Injury.Molecules (Basel, Switzerland) · 2020Article
- Long non-coding RNA CRNDE and toll-like receptor 3 correlate with disease severity, inflammation, and mortality in sepsis.Journal of clinical laboratory analysis · 2020Article
- Increased Alternative Complement Pathway Function and Improved Survival during Critical Illness.American journal of respiratory and critical care medicine · 2020Article
- Functional Evaluation of AMD-Associated Risk Variants of Complement Factor B.Investigative ophthalmology & visual science · 2020Article
- Two Gene Set Variation Index as Biomarker of Bacterial and Fungal Sepsis.BioMed research international · 2020Article
- Mechanisms of haemolysis-induced kidney injury.Nature reviews. Nephrology · 2019Review
- New insights into the immune functions of complement.Nature reviews. Immunology · 2019Review
Corrections and comments
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Authors and funding
12 authors at 6 institutions in 1 country.
Funding
Abstract
Severe sepsis involves massive activation of the innate immune system and leads to high mortality. Previous studies have demonstrated that various types of TLRs mediate a systemic inflammatory response and contribute to organ injury and mortality in animal models of severe sepsis. However, the downstream mechanisms responsible for TLR-mediated septic injury are poorly understood. In this article, we show that activation of TLR2, TLR3, and TLR4 markedly enhanced complement factor B (cfB) synthesis and release by macrophages and cardiac cells. Polymicrobial sepsis, created by cecal ligation and puncture in a mouse model, augmented cfB levels in the serum, peritoneal cavity, and major organs including the kidney and heart. Cecal ligation and puncture also led to the alternative pathway activation, C3 fragment deposition in the kidney and heart, and cfB-dependent C3dg elevation. Bacteria isolated from septic mice activated the serum alternative pathway via a factor D-dependent manner. MyD88 deletion attenuated cfB/C3 upregulation as well as cleavage induced by polymicrobial infection. Importantly, during sepsis, absence of cfB conferred a protective effect with improved survival and cardiac function and markedly attenuated acute kidney injury. cfB deletion also led to increased neutrophil migratory function during the early phase of sepsis, decreased local and systemic bacterial load, attenuated cytokine production, and reduced neutrophil reactive oxygen species production. Together, our data indicate that cfB acts as a downstream effector of TLR signaling and plays a critical role in the pathogenesis of severe bacterial sepsis.
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Registered trials
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