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Background: Quantitative assessment of macrophage accumulation is appealing in evaluating plaque inflammation. In optical coherence tomography (OCT) imaging, local macrophage clusters may be a feasible marker for macrophage quantification.
Methods: 404 patients presenting with acute coronary syndrome who underwent OCT evaluation were included. This study aims to assess the relationships between systemic inflammatory biomarkers [including monocytes, high-density lipoprotein cholesterol (HDL-C), and monocyte-to-HDL ratio (MHR)], plaque characteristics, and local macrophage clusters in coronary plaque.
Results: Macrophage clusters were present in 218 patients, with a median arc value of 72° (50°-163°). Patients with macrophage clusters showed markedly higher levels of inflammatory biomarkers and plaque vulnerability. Multivariate logistic regression analysis demonstrated that MHR, lipid index, and microchannel were independently associated with the presence of macrophage clusters. The DeLong test showed the area under the curve of the above three combined indicators was significantly larger than that of single indicators (0.774 vs. 0.692, 0.665, 0.624, respectively, < 0.001). The macrophage cluster arc correlated positively with MHR and lipid index ( = 0.219, = 0.001; and = 0.229, = 0.001, respectively). More superficial macrophage infiltration, thin cap fibroatheromas, plaque rupture, and thinner fibrous cap thickness were observed in the large macrophage cluster group (>72°) compared to the small macrophage cluster group (50°-72°). The macrophage cluster arc in the low MHR + lipid index group was significantly lower than that in the high MHR + lipid index group (68° ± 17° vs. 84° ± 26°, = 0.001). Multiple linear regression analysis demonstrated that MHR, age, and lipid index were independently associated with macrophage cluster arc. In subgroup analysis stratified by clinical presentation and high-sensitivity C-reactive protein level, higher MHR and lipid index levels were observed in large macrophage clusters than in the non-macrophage cluster group, irrespective of the inflammation background.
Conclusions: The macrophage cluster was a valuable index for quantifying local plaque inflammation. MHR, lipid index, and microchannel were independently associated with macrophage clusters. Large macrophage clusters were independently associated with high MHR and high lipid plaque burden.
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http://dx.doi.org/10.3389/fcvm.2025.1625239 | 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 PDFMol Immunol
September 2025
Department of Gastroenterology, The Sixth Affiliated Hospital of Wenzhou Medical University, Lishui People's Hospital, First Affiliated Hospital of Lishui University, Lishui, Zhejiang 323000, China. Electronic address:
Objective: Oxidative stress exerts an essential role in the pathogenesis of ulcerative colitis (UC). This study aims to unveil the heterogeneity in oxidative stress among immune cell subpopulations in UC.
Methods: Human colon epithelial cells were exposed to 100 ng/mL LPS to stimulate UC, which were administrated with antioxidants 500 mM butylated hydroxyanisole or 20 μM N-acetylcysteine.
Am J Physiol Cell Physiol
September 2025
Department of Cancer Biology, Wake Forest University School of Medicine, Winston-Salem, NC.
Cachexia, the loss of skeletal muscle mass and function with cancer, contributes to reduced life quality and worsened survival. Skeletal muscle fibrosis leads to disproportionate muscle weakness; however, the role of infiltrating immune cells and fibro-adipogenic progenitors (FAPs) in cancer-induced muscle fibrosis is not well understood. Using the C26 model of cancer cachexia, we sought to examine the changes to skeletal muscle immune cells and FAPs which contribute to excessive extracellular matrix (ECM) collagen deposition.
View Article and Find Full Text PDFJ Pathol Inform
November 2025
Pathology and Laboratory Medicine, University of Rochester Medical Center, 601 Elmwood Avenue, Rochester, NY 14642, USA.
Evaluation of tumor infiltrating lymphocytes as recommended by current guidelines is largely based on stromal regions within the tumor. In the context of epithelial malignancies, the epithelial region and the epithelial-stromal interface are not assessed, because of technical difficulties in manually discerning lymphocytes when admixed with epithelial tumor cells. The inability to quantify immune cells in epithelial-associated areas may negatively impact evaluation of patient response to immune checkpoint therapies.
View Article and Find Full Text PDFEsophagus
September 2025
Department of Surgery, Tohoku University Graduate School of Medicine, 1-1 Seiryo-Machi, Aoba-Ku, Sendai, Miyagi, Japan.
Background: The cluster of differentiation 47 (CD47)-signal regulatory protein alpha (SIRPα) axis is a key regulator of innate immune surveillance, facilitating the neoplastic evasion of macrophage-mediated phagocytosis. Although this pathway has been implicated in tumor immune escape in multiple malignancies, its clinical and prognostic significance in esophageal squamous cell carcinoma (ESCC) remain to be fully elucidated.
Methods: We retrospectively analyzed 100 patients who underwent esophagectomy for resectable ESCC.