ArticleInfection and immunity2012
Hematopoietic stem-progenitor cells restore immunoreactivity and improve survival in late sepsis.
Article in Infection and immunity, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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
33 citing papers in PubMed, 48 citations in OpenAlex.
- NuclearJournal of clinical & cellular immunology · 2025Article
- Hotairm1 Controls S100A9 Protein Phosphorylation in Myeloid-Derived Suppressor Cells during Sepsis.Journal of clinical & cellular immunology · 2023Article
- Inhibiting KDM6A Demethylase Represses Long Non-Coding RNA Hotairm1 Transcription in MDSC During Sepsis.Frontiers in immunology · 2022Article
- KDM6A Lysine Demethylase Directs Epigenetic Polarity of MDSCs during Murine Sepsis.Journal of innate immunity · 2022Article
- Swertianolin ameliorates immune dysfunction in sepsis <em>via</em> blocking the immunosuppressive function of myeloid- derived suppressor cells.European journal of histochemistry : EJH · 2021Article
- An Early Myelosuppression in the Acute Mouse Sepsis Is Partly Outcome-Dependent.Frontiers in immunology · 2021Article
- Stem Cell Therapy in Dengue Virus-Infected BALB/C Mice Improves Hepatic Injury.Frontiers in cell and developmental biology · 2021Article
- The Anti-Inflammatory Role of Bilirubin on "Two-Hit" Sepsis Animal Model.International journal of molecular sciences · 2020Article
- HuR promotes miRNA-mediated upregulation of NFI-A protein expression in MDSCs during murine sepsis.Molecular immunology · 2020Article
- Long Non-Coding RNA Hotairm1 Promotes S100A9 Support of MDSC Expansion during Sepsis.Journal of clinical & cellular immunology · 2020Article
- S100A9 maintains myeloid-derived suppressor cells in chronic sepsis by inducing miR-21 and miR-181b.Molecular immunology · 2019Article
- Attenuation of Sepsis-Induced Cardiomyopathy by Regulation of MicroRNA-23b Is Mediated Through Targeting of MyD88-Mediated NF-κB Activation.Inflammation · 2019Article
- Phagocytosis by Fibrocytes as a Mechanism to Decrease Bacterial Burden and Increase Survival in Sepsis.Shock (Augusta, Ga.) · 2019Article
- Switch of NAD Salvage toFrontiers in immunology · 2019Article
- IL-10 induces an immune repressor pathway in sepsis by promoting S100A9 nuclear localization and MDSC development.Cellular immunology · 2018Article
- Inhibition of MicroRNA-23b Attenuates Immunosuppression During Late Sepsis Through NIK, TRAF1, and XIAP.The Journal of infectious diseases · 2018Article
- Nfia deletion in myeloid cells blocks expansion of myeloid-derived suppressor cells during sepsis.Innate immunity · 2018Article
- Expression of C/EBPβ in myeloid progenitors during sepsis promotes immunosuppression.Molecular immunology · 2017Article
- Hematopoietic stem progenitor cells prevent chronic stress-induced lymphocyte apoptosis.Journal of neuroimmunology · 2017Article
- Frontline Science: Myeloid cell-specific deletion of Cebpb decreases sepsis-induced immunosuppression in mice.Journal of leukocyte biology · 2017Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Sepsis progresses from an early/acute hyperinflammatory to a late/chronic hypoinflammatory phase with immunosuppression. As a result of this phenotypic switch, mortality in late sepsis from persistent primary infection or opportunistic new infection often exceeds that in acute sepsis. Emerging data support that persistence of the hypoinflammatory (hyporesponsive) effector immune cells during late sepsis might involve alterations in myeloid differentiation/maturation that generate circulating repressor macrophages that do not readily clear active infection. Here, we used a cecal ligation and puncture (CLP) murine model of prolonged sepsis to show that adoptive transfer of CD34(+) hematopoietic stem-progenitor cells after CLP improves long-term survival by 65%. CD34(+) cell transfer corrected the immunosuppression of late sepsis by (i) producing significantly higher levels of proinflammatory mediators upon ex vivo stimulation with the Toll-like receptor 4 (TLR4) agonist lipopolysaccharide, (ii) enhancing phagocytic activity of peritoneal macrophages, and (iii) clearing bacterial peritonitis. Improved immunity by CD34(+) cell transfer decreased inflammatory peritoneal exudate of surviving late-sepsis mice. Cell tracking experiments showed that the transferred CD34(+) cells first appeared in the bone marrow and then homed to the spleen and peritoneum. Because CD34(+) cells did not affect the early-phase hyperinflammatory response, it is likely that the newly incorporated pluripotent CD34(+) cells differentiated into competent immune cells in blood and tissue, thereby reversing or replacing the hyporesponsive endotoxin-tolerant cells that occur and persist after the initiation of early 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.