ArticleJournal of immunology (Baltimore, Md. : 1950)2011
Distinct different contributions of the alternative and classical complement activation pathway for the innate host response during sepsis.
Article in Journal of immunology (Baltimore, Md. : 1950), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.
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Who cites it
21 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.
- C1q as a target molecule to treat human disease: What do mouse studies teach us?Frontiers in immunology · 2022Pooled it
- A Targeted Blockade of Terminal C5a Is Critical to Management of Sepsis and Acute Respiratory Distress Syndrome: The Mechanism of Action of Vilobelimab.International journal of molecular sciences · 2025Review
- Novel broadly reactive monoclonal antibody protects againstInfection and immunity · 2025Article
- Bacterial and host interactions inFrontiers in microbiology · 2025Review
- Adipsin improves diabetic hindlimb ischemia through SERPINE1 dependent angiogenesis.Cardiovascular diabetology · 2024Article
- The complement system: A key player in the host response to infections.European journal of immunology · 2024Review
- Exosomes derived from pericardial adipose tissues attenuate cardiac remodeling following myocardial infarction by Adipsin-regulated iron homeostasis.Frontiers in cardiovascular medicine · 2022Article
- Elevated Adipsin and Reduced C5a Levels in the Maternal Serum and Follicular Fluid During Implantation Are Associated With Successful Pregnancy in Obese Women.Frontiers in endocrinology · 2022Article
- Complement factor D is linked to platelet activation in human and rodent sepsis.Intensive care medicine experimental · 2021Article
- Use of IFNγ/IL10 Ratio for Stratification of Hydrocortisone Therapy in Patients With Septic Shock.Frontiers in immunology · 2021Article
- High Endurance Elite Athletes Show Age-dependent Lower Levels of Circulating Complements Compared to Low/Moderate Endurance Elite Athletes.Frontiers in molecular biosciences · 2021Article
- Molecular Analysis of the Contribution of Alkaline Protease A and Elastase B to the Virulence ofFrontiers in cellular and infection microbiology · 2021Article
- Saponins as adipokines modulator: A possible therapeutic intervention for type 2 diabetes.World journal of diabetes · 2017Review
- Article
- C1q Deficiency Promotes Pulmonary Vascular Inflammation and Enhances the Susceptibility of the Lung Endothelium to Injury.The Journal of biological chemistry · 2015Article
- Regulation of the gut microbiota by the mucosal immune system in mice.International immunology · 2014Review
- Article
- Complement factor B is the downstream effector of TLRs and plays an important role in a mouse model of severe sepsis.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- OPSI threat in hematological patients.Translational medicine @ UniSa · 2013Article
- Complement-dependent injury and protection in a murine model of acute dextran sulfate sodium-induced colitis.Journal of immunology (Baltimore, Md. : 1950) · 2012Article
Corrections and comments
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Authors and funding
14 authors at 5 institutions in 2 countries.
Funding
Abstract
Complement activation represents a crucial innate defense mechanism to invading microorganisms, but there is an eminent lack of understanding of the separate contribution of the different complement activation pathways to the host response during sepsis. We therefore investigated different innate host immune responses during cecal ligation and puncture (CLP)-induced sepsis in mice lacking either the alternative (fD(-/-)) or classical (C1q(-/-)) complement activation pathway. Both knockout mice strains showed a significantly reduced survival and increased organ dysfunction when compared with control mice. Surprisingly, fD(-/-) mice demonstrated a compensated bacterial clearance capacity as control mice at 6 h post CLP, whereas C1q(-/-) mice were already overwhelmed by bacterial growth at this time point. Interestingly, at 24 h after CLP, fD(-/-) mice failed to clear bacteria in a way comparable to control mice. However, both knockout mice strains showed compromised C3 cleavage during sepsis. Investigating potential causes for this discrepancy, we were able to demonstrate that despite normal bacterial clearance capacity early during the onset of sepsis, fD(-/-) mice displayed increased inflammatory cytokine generation and neutrophil recruitment into lungs and blood when compared with both control- and C1q(-/-) mice, indicating a potential loss of control over these immune responses. Further in vitro experiments revealed a strongly increased Nf-κB activation capacity in isolated neutrophils from fD(-/-) mice, supporting this hypothesis. Our results provide evidence for the new concept that the alternative complement activation pathway exerts a distinctly different contribution to the innate host response during sepsis when compared with the classical pathway.
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Registered trials
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