ReviewBiomolecules2023
Infection, Inflammation, and Immunity in Sepsis.
Review in Biomolecules, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 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.
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
39 citing papers in PubMed, 59 citations in OpenAlex.
- AA in Rheumatoid Arthritis and Lupus.Reviews of physiology, biochemistry and pharmacology · 2027Review
- Introduction.Reviews of physiology, biochemistry and pharmacology · 2027Article
- AA-Induced Lipid Peroxidation at the Center of Tumor Cell Apoptosis and Ferroptosis.Reviews of physiology, biochemistry and pharmacology · 2027Review
- Physiological Significance and Functions of AA.Reviews of physiology, biochemistry and pharmacology · 2027Review
- BIENs: biomimetic interface encoding on FeMikrochimica acta · 2026Article
- How does OA affect sepsis? An observational study and Mendelian randomization mediation analysis.Osteoarthritis and cartilage open · 2026Article
- From Glycocalyx Shedding to Microvascular Collapse in Sepsis: Endothelial Pathophysiology, Organ Dysfunction, and Mechanistic Biomarkers.Pathophysiology : the official journal of the International Society for Pathophysiology · 2026Review
- Berbamine modulates pro-inflammatory cytokines and alleviates sepsis-induced acute myocardial injury in mice: role of NLRP3/GSDMD signaling axis.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Article
- The "cytokine storm" in infection and sepsis: win the battle but lose the war.Military Medical Research · 2026Review
- Fuzheng Jiedu formula attenuates acute pneumonia by coordinated regulation of macrophage NLRP3 inflammasome and neutrophil NETs.Chinese medicine · 2026Article
- TUDCA-3S is Associated with Acute Pancreatitis Severity and Pro-Inflammatory Macrophage Activation Involving S100A8/IL-17 Signaling.Journal of inflammation research · 2026Article
- Single-Cell Profiling Identifies JUNB/SPI1-Driven Inflammatory Programs and Novel Communication Axes in Myeloid Cells of SepsisEndocrine, metabolic & immune disorders drug targets · 2026Article
- MFSD2A: a molecular nexus linking blood-brain barrier, lipid metabolism, and ischemia-reperfusion injury.Cellular & molecular biology letters · 2025Review
- Lipopolysaccharide Potentiates Platelet Aggregation in Association with Apoptosis Through a Novel TLR4-Bax/Bcl-2-Mitochondrial Dysfunction Axis in Humans.Biomolecules · 2025Article
- Function of epigenetic modifications in wound healing and potential therapies (Review).International journal of molecular medicine · 2025Review
- Sepsis toxicity network reconstruction-Dynamic signaling and multi-organ injury: A review.Biomolecules & biomedicine · 2025Review
- The S2 Glycoprotein Subunit Determines Intestinal Tropism in Infectious Bronchitis Virus.Microorganisms · 2025Article
- Preoperative inflammatory markers in pediatric appendicitis: associations with disease severity, postoperative recovery, pain, and surgical outcomes.BMC pediatrics · 2025Article
- Article
Corrections and comments
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Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sepsis is triggered by microbial infection, injury, or even major surgery. Both innate and adaptive immune systems are involved in its pathogenesis. Cytoplasmic presence of DNA or RNA of the invading organisms or damaged nuclear material (in the form of micronucleus in the cytoplasm) in the host cell need to be eliminated by various nucleases; failure to do so leads to the triggering of inflammation by the cellular cGAS-STING system, which induces the release of IL-6, TNF-α, and IFNs. These cytokines activate phospholipase A2 (PLA2), leading to the release of polyunsaturated fatty acids (PUFAs), gamma-linolenic acid (GLA), arachidonic acid (AA), eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA), which form precursors to various pro- and anti-inflammatory eicosanoids. On the other hand, corticosteroids inhibit PLA2 activity and, thus, suppress the release of GLA, AA, EPA, and DHA. PUFAs and their metabolites have a negative regulatory action on the cGAS-STING pathway and, thus, suppress the inflammatory process and initiate inflammation resolution. Pro-inflammatory cytokines and corticosteroids (corticosteroids > IL-6, TNF-α) suppress desaturases, which results in decreased formation of GLA, AA, and other PUFAs from the dietary essential fatty acids (EFAs). A deficiency of GLA, AA, EPA, and DHA results in decreased production of anti-inflammatory eicosanoids and failure to suppress the cGAS-STING system. This results in the continuation of the inflammatory process. Thus, altered concentrations of PUFAs and their metabolites, and failure to suppress the cGAS-STING system at an appropriate time, leads to the onset of sepsis. Similar abnormalities are also seen in radiation-induced inflammation. These results imply that timely administration of GLA, AA, EPA, and DHA, in combination with corticosteroids and anti-IL-6 and anti-TNF-α antibodies, may be of benefit in mitigating radiation-induced damage and sepsis.
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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.