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: Neutrophils are key innate immune cells in peripheral blood. In recent years, sub-populations of neutrophils have been identified. In addition to the normal-density neutrophils (NDNs) in both healthy subjects and patients, low-density neutrophils (LDNs) were described in chronic inflammation and cancer. In lung transplants (LTx), neutrophils play crucial roles in reperfusion injury, acute rejection, and chronic lung allograft dysfunction. Our pilot study examines neutrophil subsets and function in LTx recipients during the first post-transplant year. : We collected blood from 11 LTx recipients at various intervals. LDNs and normal-density neutrophils (NDNs) were isolated. The production of reactive oxygen species (ROS) by NDNs was measured after PMA activation using a Luminol-HRP assay. Neutrophil phenotypic markers were analyzed with flow cytometry. : The LDN-to-NDN ratio increased at 3 and 6 months post-transplant. Expression levels of CD62-L (aging marker), PDL-1 (immune checkpoint), CD15 (maturation), and CXCR4 (homeostasis regulator) showed modulation. Interestingly, ROS production by NDNs was mildly elevated at baseline, reduced at 6 months, and returned to baseline levels by 9 months post-transplant. : Neutrophils exhibit dynamic changes in the first post-LTx year. Investigating neutrophil plasticity could reveal clinically relevant biomarkers and facilitate the development of diagnostic and therapeutic tools in LTx.
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http://dx.doi.org/10.3390/jcm14082660 | DOI Listing |
Nat Commun
September 2025
Institute of Computational Biology, German Research Center for Environmental Health, Helmholtz Zentrum München, Neuherberg, Germany.
Atherosclerosis, a major cause of cardiovascular diseases, is characterized by the buildup of lipids and chronic inflammation in the arteries, leading to plaque formation and potential rupture. Despite recent advances in single-cell transcriptomics (scRNA-seq), the underlying immune mechanisms and transformations in structural cells driving plaque progression remain incompletely defined. Existing datasets often lack comprehensive coverage and consistent annotations, limiting the utility of downstream analyses.
View Article and Find Full Text PDFImmunity
September 2025
Research Institute of Molecular Pathology (IMP), Vienna BioCenter (VBC), Vienna, Austria. Electronic address:
In a recent issue of Nature, Adrover et al. report a neutrophil subset that induces pleomorphic tumor necrosis through neutrophil extracellular trap (NET)-mediated vascular occlusion. This process drives epithelial-to-mesenchymal transition (EMT) and metastasis of perinecrotic cancer cells, reframing necrosis as an active process and uncovering targetable mechanisms to combat cancer dissemination.
View Article and Find Full Text PDFInt J Gen Med
September 2025
Department of Geriatrics, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, 610072, People's Republic of China.
Background: Sepsis is characterized by profound immune and metabolic perturbations, with glycolysis serving as a pivotal modulator of immune responses. However, the molecular mechanisms linking glycolytic reprogramming to immune dysfunction remain poorly defined.
Methods: Transcriptomic profiles of sepsis were obtained from the Gene Expression Omnibus.
Infect Immun
September 2025
Institute of Medical Microbiology and Hospital Hygiene, Heinrich Heine University, Düsseldorf, Germany.
Lymphotoxin β receptor (LTβR/TNFRSF3) signaling plays a crucial role in immune defense. Notably, LTβR-deficient (LTβR) mice exhibit severe defects in innate and adaptive immunity against various pathogens and succumb to infection. Here, we investigated the bone marrow (BM) and peritoneal cavity (PerC) compartments of LTβR mice during infection, demonstrating perturbed B-cell and T-cell subpopulations in the absence of LTβR signaling.
View Article and Find Full Text PDFJ Burn Care Res
September 2025
Department of Burn Surgery, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, China.
Background: Burn injuries trigger complex immune responses and gene expression changes, impacting wound healing and systemic inflammation. Understanding these changes is crucial for identifying biomarkers and therapeutic targets.
Methods: We analyzed two GEO datasets (wound tissue (GSE8056) and blood (GSE37069)) to identify differentially expressed genes (DEGs) in burn injury samples versus controls.