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Arum maculatum agglutinin (AMA) is a monocot lectin isolated from tubers of Arum maculatum L. (Araceae) which exhibits different specificity towards oligo-mannosidic-type and N-acetyllactosaminic-type glycans. We have investigated the effect of this lectin on the cells of the immune system. Models of neutrophil migration in vivo, neutrophil chemotaxis in vitro and macrophage cultures were used to study the lectin inflammatory activity. When administered into rat peritoneal cavities, AMA (80, 200 and 500 microg/mL/cavity) induced significant and dose-dependent neutrophil migration. This effect was inhibited by incubation with alpha-methyl-d-mannoside. A 83% depletion in the number of resident cells following peritoneal lavage did not reduce the AMA-induced neutrophil migration, as compared to sham animals (not washed). However, pre-treatment with 3% thioglycolate which increases the peritoneal macrophage population by 236%, enhanced the neutrophil migration induced by AMA (200 microg/mL/cavity) (119%, p < 0.05). Reduction of peritoneal mast cell population by chronic treatment of cavities with compound 48/80 did not modify AMA-induced neutrophil migration. The neutrophil chemotaxy assay in vitro shows that the lectin (300 microg/mL) induces neutrophil chemotaxy (368% p < 0.05) compared to RPMI. Finally, injection into peritoneal cavities of supernatants from macrophage cultures obtained after stimulation with AMA (300 microg/mL) enhanced neutrophil migration (110% p < 0.05). Summarizing, our data suggest that A. maculatum agglutinin presents pro-inflammatory activity, inducing neutrophil migration by two ways, one which is independent on resident cells and another one dependent on the presence of these cells.
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http://dx.doi.org/10.1016/j.biocel.2005.02.027 | DOI Listing |
Front Immunol
September 2025
Institute of Pulmonary Medicine, Hadassah Hebrew University Medical Center, Jerusalem, Israel.
Neutrophil extracellular traps (NETs) are DNA-protein structures released during a form of programmed neutrophil death known as NETosis. While NETs have been implicated in both tumor inhibition and promotion, their functional role in cancer remains ambiguous. In this study, we compared the NET-forming capacity and functional effects of NETs derived from lung cancer (LC) patients and healthy donors (H).
View Article and Find Full Text PDFInt Immunopharmacol
September 2025
Department of Pathology, The Second Affiliated Hospital of Anhui Medical University, Hefei, Anhui 230601, PR China; Department of Pathology, The First Affiliated Hospital of Anhui Medical University, Hefei, Anhui 230061, PR China. Electronic address:
Tumor-associated neutrophils (TANs) play a critical role in breast cancer progression. This study demonstrated that high CD66b TANs infiltration correlated with poor disease-free survival (DFS) and promoted proliferation, migration, and invasion of breast cancer cells in vitro. Conversely, the immune-related long non-coding RNA C6orf99 was downregulated in breast cancer and associated with favorable DFS.
View Article and Find Full Text PDFInfect 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 Gastroenterol
September 2025
Department of General Surgery (Hepatopancreatobiliary Surgery), Department of Biliary-Pancreatic Center, The Affiliated Hospital of Southwest Medical University, 25 Taiping Street, Jiangyang District, Luzhou City, 646000, Sichuan Province, China.
Background And Aims: Inflammatory cell infiltration in the liver is a hallmark of metabolic dysfunction-associated fatty liver disease (MAFLD). However, the pathological events that trigger the infiltration of inflammatory cells to mediate MAFLD pathogenesis remains poorly understood. This study aims to investigate the function and mechanism of Hic-5 on hepatic inflammation of MAFLD.
View Article and Find Full Text PDFImmunology
September 2025
Department of Biochemical Science and Technology, National Taiwan University, Taipei, Taiwan, ROC.
Enolase-1 (ENO1) is a moonlighting protein with multiple functions. When expressed on the cell surface, ENO1 binds plasminogen (PLG) and promotes cell migration by facilitating plasmin (PLM)-mediated extracellular matrix degradation. Here, we observed that inflammatory stimulation significantly upregulated ENO1 expression on the neutrophil surface, both in vitro and in vivo.
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