ArticleJournal of immunology (Baltimore, Md. : 1950)2012
Complement-dependent injury and protection in a murine model of acute dextran sulfate sodium-induced colitis.
Article in Journal of immunology (Baltimore, Md. : 1950), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.
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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
25 citing papers in PubMed, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.
- C1q as a target molecule to treat human disease: What do mouse studies teach us?Frontiers in immunology · 2022Pooled it
- Serum proteomics in paediatric inflammatory bowel disease from a case-control study: biomarker discovery and ulcerative colitis-Crohn's disease differentiation.EBioMedicine · 2026Article
- The role of the complement system in gastrointestinal-related diseases.Frontiers in immunology · 2026Review
- Mucosally sourced complement factor B modulates the host response to colitis.bioRxiv : the preprint server for biology · 2026Article
- Dual roles of complement in ulcerative colitis: insights from clinical studies and animal research.European journal of medical research · 2025Review
- The complement system in intestinal inflammation and cancer.The Journal of clinical investigation · 2025Review
- Enigmatic Roles of Complement Anaphylatoxin Signaling in Health and Disease.Immune network · 2025Review
- Proteomic profile of human colon organoids: effects of a multi-mineral intervention alone and in the presence of pro-inflammatory and anti-inflammatory treatments.Frontiers in gastroenterology (Lausanne, Switzerland) · 2025Article
- A Novel Probiotic Combination Ameliorates Crohn's Disease-Like Ileitis by Increasing Short-Chain Fatty Acid Production and Modulating Essential Adaptive Immune Pathways.Inflammatory bowel diseases · 2023Article
- An Extremes of Phenotype Approach Confirms Significant Genetic Heterogeneity in Patients with Ulcerative Colitis.Journal of Crohn's & colitis · 2023Article
- The Dynamic Change of Gene-Regulated Networks in Cashmere Goat Skin with Seasonal Variation.Biochemical genetics · 2022Article
- Evaluation of AIF-1 (Allograft Inflammatory Factor-1) as a Biomarker of Crohn's Disease Severity.Biomedicines · 2022Article
- Upregulation of complement C1q reflects mucosal regeneration in a mouse model of colitis.Medical molecular morphology · 2021Article
- A Protective and Pathogenic Role for Complement During AcuteFrontiers in cellular and infection microbiology · 2021Review
- Deciphering microbiome and neuroactive immune gene interactions in schizophrenia.Neurobiology of disease · 2020Review
- Tissue-targeted complement therapeutics.Molecular immunology · 2018Review
- Ficolin-A/2, acting as a new regulator of macrophage polarization, mediates the inflammatory response in experimental mouse colitis.Immunology · 2017Article
- Properdin deficiency protects from 5-fluorouracil-induced small intestinal mucositis in a complement activation-independent, interleukin-10-dependent mechanism.Clinical and experimental immunology · 2017Article
- Galectin-3 suppresses mucosal inflammation and reduces disease severity in experimental colitis.Journal of molecular medicine (Berlin, Germany) · 2016Article
- Regulation of the alternative pathway of complement modulates injury and immunity in a chronic model of dextran sulphate sodium-induced colitis.Clinical and experimental immunology · 2015Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Complement plays a key role in the pathophysiology of many inflammatory diseases, and in this study, we investigated the role of complement in the pathogenesis of inflammatory bowel disease. Compared to wild-type mice, mice deficient in C3 or factor B were protected from acute dextran sulfate sodium (DSS)-induced colitis. C1q/mannose-binding lectin (MBL) double-deficient mice, however, exhibited more severe colitis than wild-type mice. When mice were allowed to recover after DSS treatment, all C1q/MBL(-/-) mice died by day 2 of recovery period, and, surprisingly, all C3(-/-) and factor B(-/-) mice died by day 5. Serum endotoxin levels were significantly increased in complement-deficient mice prior to death, particularly in C1q/MBL(-/-) mice, and antibiotic treatment prevented the lethal effect of DSS in all complement-deficient mice. In contrast to complement deficiency, targeted complement inhibition with either complement receptor 2 (CR2)-Crry (blocks all pathways at C3 activation) or CR2-factor H (blocks alternative pathway) was highly protective at treating established acute colitis. Endotoxin levels remained low in complement-inhibited mice, and complement inhibition also reduced inflammatory cytokines, leukocyte infiltration, and tissue injury while improving wound repair and mucosal healing. CR2-factor H provided more effective protection than CR2-Crry. Thus, complement has both pathogenic and protective roles in acute DSS-induced colitis, and whereas the alternative pathway appears to play a key role in tissue inflammation and injury, the classical/lectin pathway provides important protection in terms of host defense and wound repair. Targeted inhibition of the alternative pathway may represent a therapeutic modality for treating acute phases of inflammatory bowel disease.
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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.