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Lithium, Inflammation and Neuroinflammation with Emphasis on Bipolar Disorder-A Narrative Review.
Int J Mol Sci
December 2024
Department of Clinical Biochemistry and Pharmacology, Faculty of Health Sciences, Zlotowski Center for Neuroscience and Zelman Center-The School of Brain Sciences and Cognition, Ben-Gurion University of the Negev, Beer-Sheva 8410501, Israel.
This narrative review examines lithium's effects on immune function, inflammation and cell survival, particularly in bipolar disorder (BD) in in vitro studies, animal models and clinical studies. In vitro studies show that high lithium concentrations (5 mM, beyond the therapeutic window) reduce interleukin (IL)-1β production in monocytes and enhance T-lymphocyte resistance, suggesting a protective role against cell death. Lithium modulates oxidative stress in lipopolysaccharide (LPS)-activated macrophages by inhibiting nuclear factor (NF)-ƙB activity and reducing nitric oxide production.
View Article and Find Full Text PDFTime-dependent variation in immunoparalysis biomarkers among patients with sepsis and critical illness.
Front Immunol
December 2024
Department of Anesthesiology and Perioperative Medicine, Penn State Medical Center, Hershey, PA, United States.
Introduction: Immunoparalysis is a state of immune dysfunction characterized by a marked reduction in the immune system's responsiveness, often observed following severe infections, trauma, or critical illness. This study aimed to perform a longitudinal assessment of immune function over the initial two weeks following the onset of sepsis and critical illness.
Methods: We compared ex vivo-stimulated cytokine release from whole blood of critically ill patients to traditional markers of immunoparalysis, including monocyte Human Leukocyte Antigen (mHLA)-DR expression and absolute lymphocyte count (ALC).
Development of a Simple IFN-γ Release Whole Blood Assay for the Assessment of Specific Cellular Immunity in Dogs.
Animals (Basel)
November 2024
Departament de Medicina i Cirurgia Animals, Facultat de Veterinària, Universitat Autònoma de Barcelona (UAB), 08193 Bellaterra, Spain.
Canine leishmaniosis (CanL) is a zoonotic disease caused by , where increased interferon-gamma (IFN-γ) levels are associated with controlling the infection and mild to moderate disease. Therefore, monitoring IFN-γ concentrations is essential for monitoring the immune responses in CanL. This study compared a faster, cost-effective IFN-γ release whole blood assay in tubes (WBA-T) with a standardized version (WBA-S) in 41 dogs at different states of infection.
View Article and Find Full Text PDFEffect of decitabine on PD-L2 methylation in whole blood of iodine-induced autoimmune thyroiditis rats.
Ecotoxicol Environ Saf
December 2024
Department of Preventive Medicine, Qiqihar Medical University, Qiqihar, Heilongjiang, China. Electronic address:
Article Synopsis
- Excessive iodine intake can lead to autoimmune thyroiditis (AIT), with methylation changes in the PD-L2 gene potentially playing a crucial role in this condition.
- Researchers used Decitabine, a DNA methyltransferase inhibitor, in an experimental model to explore the effects on AIT, involving various biochemical and molecular techniques to assess thyroid function and immune responses.
- Results indicated that iodine-induced AIT was associated with decreased PD-L2 methylation and increased inflammatory markers, while treatment with Decitabine improved thyroid function trends and altered PD-L2 expression, though more safety evaluations are needed for this potential treatment.
[Evaluation of whole blood immunoreactivity].
Khirurgiia (Mosk)
December 2024
Petrovsky National Research Center of Surgery, Moscow, Russia.
To assess cellular immunoreactivity, lipopolysaccharide (LPS), Concanavalin A (Con A), or LPS together with Con A was added to the whole blood for 18 hours. LPS preferentially stimulated release of tumor necrosis factor-alfa (TNF-α), interleukin-6 (IL-6), IL-10 and vascular endothelial growth factor (VEGF) by blood cells, whereas Con A significantly enhanced secretion of interferon-gamma (IFN-gamma) and IL-2. Addition of heparin to blood slightly decreased cellular secretion of IL-2 and VEGF, but not other cytokines.
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