ArticleShock (Augusta, Ga.)2016
TLR2 Regulates Complement-Mediated Inflammation Induced by Blood Loss During Hemorrhage.
Article in Shock (Augusta, Ga.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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.
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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
8 citing papers in PubMed, 14 citations in OpenAlex.
- Article
- Botulinum neurotoxin A ameliorates depressive-like behavior in a reserpine-induced Parkinson's disease mouse model via suppressing hippocampal microglial engulfment and neuroinflammation.Acta pharmacologica Sinica · 2023Article
- METTL3 Regulates the Inflammatory Response in CPB2 Toxin-Exposed IPEC-J2 Cells through the TLR2/NF-κB Signaling Pathway.International journal of molecular sciences · 2022Article
- Early Post-ischemic Brain Glucose Metabolism Is Dependent on Function of TLR2: a Study Using [Molecular imaging and biology · 2022Article
- Article
- Innate immunity and immunotherapy for hemorrhagic shock.Frontiers in immunology · 2022Review
- Hemorrhagic shock induces renal complement activation.European journal of trauma and emergency surgery : official publication of the European Trauma Society · 2021Article
- Protective Effects of the Complement Inhibitor Compstatin CP40 in Hemorrhagic Shock.Shock (Augusta, Ga.) · 2019Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Hemorrhagic shock resulting from blood loss directs the majority of the blood to the vital organs, dramatically reducing blood flow to the intestines and resulting in damage and inflammation. The excessive intestinal inflammatory response includes pro-inflammatory cytokines and complement activation, although the mechanism is not clear. Toll-like receptors play a vital role in the innate immune response and toll-like receptor 2 (TLR2) is required for intestinal ischemia/reperfusion-induced injury. We hypothesized that TLR2 plays an integral role in the intestinal inflammatory response after hemorrhage and subjected C57Bl/6 wild-type and Tlr2(-/-) mice to atraumatic loss of ∼30% total blood volume. Two hours after blood removal, the intestinal injury and inflammation were assessed. We demonstrate that compared with wild-type control mice, Tlr2(-/-) mice sustain less intestinal damage and inflammation. Importantly, TLR2 regulated eicosanoid and complement activation and IL-12 and TNFα secretions, indicating interactions between TLR2 and complement in response to significant blood loss.
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Registered trials
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