ReviewBiomedicines2024
Immunosuppression in Sepsis: Biomarkers and Specialized Pro-Resolving Mediators.
Review in Biomedicines, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
24 citing papers in PubMed, 33 citations in OpenAlex.
- Targeting the NR1D1-IGF2BP2-V-ATPase Axis With Hybrid Nanovesicles Restores Macrophage Rhythms to Reverse Sepsis-Induced Immunosuppression.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Review
- Dexmedetomidine attenuates sepsis-associated NET formation and Th17 polarization through α2-adrenergic receptor-associated regulation of hepatic HPD.Archives of pharmacal research · 2026Article
- FOLR3+neutrophils contribute to sepsis by exacerbating hyper-inflammation.Genes and immunity · 2026Article
- Biomimetic Targeted Drug Delivery for Liver Failure in Abdominal Sepsis: Focus on Autologous Erythrocyte Ghosts.International journal of molecular sciences · 2026Review
- Metabolic and post-translational modifications in sepsis-associated immune dysfunction: a conceptual framework.Frontiers in immunology · 2026Review
- Crosstalk between innate immune signaling pathways and integrated TLR, NLRP3 inflammasome, cGAS-STING, and NF-κB networks in sepsis.Frontiers in cell and developmental biology · 2026Review
- The Emerging Roles of Resolvins: Potential Diagnostic Biomarkers for Cardiovascular Diseases.Current cardiology reviews · 2026Review
- Reactive oxygen species elevations in human immune cell subsets during sepsis are mitigated by norepinephrine and N-acetylcysteine.World journal of critical care medicine · 2025Article
- Immunomodulatory Nanozymes Eradicate Intracellular Infections and Rescue Immunoparalysis for Treating Multidrug-Resistant Bacterial Sepsis.Exploration (Beijing, China) · 2025Article
- Immunodynamic Disruption in Sepsis: Mechanisms and Strategies for Personalized Immunomodulation.Biomedicines · 2025Review
- Integrated multiomics and Mendelian randomization identify CHIT1 as a novel sepsis biomarker and therapeutic target.Scientific reports · 2025Article
- ITGB2 and ICAM3 predict increased survival of sepsis with decreased intercellular communication in cytotoxic CD8+ T cells.Scientific reports · 2025Article
- Oxylipins as canine sepsis indicators in vivo and in ex vivo skin organ culture model.Scientific reports · 2025Article
- Molecular Biomarkers and More Efficient Therapies for Sepsis.Biomedicines · 2025Article
- Dysregulation of neutrophil in sepsis: recent insights and advances.Cell communication and signaling : CCS · 2025Review
- Targeting the immuno-inflammatory-microbial network: a key strategy for sepsis treatment.Frontiers in immunology · 2025Review
- Relationship between peripheral bloodFrontiers in immunology · 2025Article
- The potential of exogenous specialized pro-resolving mediators in protecting against sepsis-associated lung injury: a review.Frontiers in pharmacology · 2025Review
- Tim-3 pathway dysregulation and targeting in sepsis-induced immunosuppression.European journal of medical research · 2024Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Severe infection can lead to sepsis. In sepsis, the host mounts an inappropriately large inflammatory response in an attempt to clear the invading pathogen. This sustained high level of inflammation may cause tissue injury and organ failure. Later in sepsis, a paradoxical immunosuppression occurs, where the host is unable to clear the preexisting infection and is susceptible to secondary infections. A major issue with sepsis treatment is that it is difficult for physicians to ascertain which stage of sepsis the patient is in. Sepsis treatment will depend on the patient's immune status across the spectrum of the disease, and these immune statuses are nearly polar opposites in the early and late stages of sepsis. Furthermore, there is no approved treatment that can resolve inflammation without contributing to immunosuppression within the host. Here, we review the major mechanisms of sepsis-induced immunosuppression and the biomarkers of the immunosuppressive phase of sepsis. We focused on reviewing three main mechanisms of immunosuppression in sepsis. These are lymphocyte apoptosis, monocyte/macrophage exhaustion, and increased migration of myeloid-derived suppressor cells (MDSCs). The biomarkers of septic immunosuppression that we discuss include increased MDSC production/migration and IL-10 levels, decreased lymphocyte counts and HLA-DR expression, and increased GPR18 expression. We also review the literature on the use of specialized pro-resolving mediators (SPMs) in different models of infection and/or sepsis, as these compounds have been reported to resolve inflammation without being immunosuppressive. To obtain the necessary information, we searched the PubMed database using the keywords sepsis, lymphocyte apoptosis, macrophage exhaustion, MDSCs, biomarkers, and SPMs.
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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.