Corrigendum to “Expression of CXCR1 (IL-8 receptor A) in splenic, peritoneal macrophages and resident bone marrow cells after acute live or heat killed Staphylococcus aureus stimulation in mice”[Microb. Pathog. 109 (2017) 131–150]

Abstract Radioiodinated L-cell-derived colony-stimulating factor (CSF) was used to characterize the binding reaction to murine bone marrow cells. The major increment in cell-associated radioactivity occurred over 24 hr incubation at 37 degrees C, but virtually no binding was observed at 4 degrees C. The reaction was saturable with approximately 1 ng/ml of purified CSF. Unlabeled CSF prevented the binding, whereas a number of other hormones and proteins did not compete for CSF uptake. Further specificity studies showed virtually no binding to human bone marrow, which is unresponsive to this form of murine CSF. Minimal CSF uptake was noted with murine peritoneal macrophages, but virtually no binding was detected with thymic, lymph node, liver, or kidney cells. The marrow cell interaction with tracer appeared to require a new protein synthesis, as the binding was prevented by cycloheximide or puromycin. Preincubation of marrow cells in medium devoid of CSF increased the degree of binding after 1 hr exposure to the tracer. This suggests that CSF binding sites may be occupied or perhaps decreased in response to ambient levels of CSF in vivo. Approximately 70% of the bound radioactivity was detected in the cytoplasm at 24 hr. This material was partially degraded as judged by a decrease in molecular weight from approximately 62,000 to 2 peaks of approximately 32,000 and approximately 49,000, but 72% of the binding activity was retained. After plateau binding was achieved, greater than 80% of the radioactivity released into the medium was degraded into biologically inactive peptides with molecular weights less than 10,000. These findings suggest that the interaction of CSF with marrow cells is characterized by binding with subsequent internalization and metabolic degradation into portions of the molecule that are devoid of biologic activity.

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Transformation of Mouse Peritoneal Macrophages and Bone Marrow Cells by Simian Virus 40

Microbiology and Immunology ◽

10.1111/j.1348-0421.1980.tb00573.x ◽

1980 ◽

Vol 24 (2) ◽

pp. 155-167 ◽

Cited By ~ 14

Author(s):

Hisao Takayama

Keyword(s):

Bone Marrow ◽

Bone Marrow Cells ◽

Simian Virus 40 ◽

Peritoneal Macrophages ◽

Simian Virus ◽

Mouse Peritoneal Macrophages ◽

Marrow Cells

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Effect of oral administration of the fresh juice of Bamboo (Bambusa vulgaris) young shoots on enumeration of bone marrow cells, platelets, splenocyte and phagocytic activity of peritoneal macrophages of rats

Phytomedicine Plus ◽

10.1016/j.phyplu.2021.100059 ◽

2021 ◽

pp. 100059

Author(s):

Nayanathara Thathsarani ◽

Chanika D. Jayasinghe ◽

Uthpala Jayawardena ◽

Nayanakanthi Nilakarawasam

Keyword(s):

Bone Marrow ◽

Oral Administration ◽

Phagocytic Activity ◽

Bone Marrow Cells ◽

Peritoneal Macrophages ◽

Bambusa Vulgaris ◽

Marrow Cells

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In Vitro 3D Staphylococcus aureus Abscess Communities Induce Bone Marrow Cells to Expand into Myeloid-Derived Suppressor Cells

Pathogens ◽

10.3390/pathogens10111446 ◽

2021 ◽

Vol 10 (11) ◽

pp. 1446

Author(s):

Marloes I. Hofstee ◽

Anja Heider ◽

Sonja Häckel ◽

Caroline Constant ◽

Martijn Riool ◽

...

Keyword(s):

Staphylococcus Aureus ◽

Bone Marrow ◽

T Cell ◽

Bone Marrow Cells ◽

Suppressor Cells ◽

Myeloid Derived Suppressor Cells ◽

Cell Numbers ◽

Biomarker Analysis ◽

Marrow Cells

Staphylococcus aureus is the main causative pathogen of subcutaneous, bone, and implant-related infections, forming structures known as staphylococcal abscess communities (SACs) within tissues that also contain immunosuppressive myeloid-derived suppressor cells (MDSCs). Although both SACs and MDSCs are present in chronic S. aureus infections, it remains unknown whether SACs directly trigger MDSC expansion. To investigate this, a previously developed 3D in vitro SAC model was co-cultured with murine and human bone marrow cells. Subsequently, it was shown that SAC-exposed human CD11blow/− myeloid cells or SAC-exposed murine CD11b+ Gr-1+ cells were immunosuppressive mainly by reducing absolute CD4+ and CD8α+ T cell numbers, as shown in T cell proliferation assays and with flow cytometry. Monocytic MDSCs from mice with an S. aureus bone infection also strongly reduced CD4+ and CD8α+ T cell numbers. Using protein biomarker analysis and an immunoassay, we detected in SAC–bone marrow co-cultures high levels of GM-CSF, IL-6, VEGF, IL-1β, TNFα, IL-10, and TGF-β. Furthermore, SAC-exposed neutrophils expressed Arg-1 and SAC-exposed monocytes expressed Arg-1 and iNOS, as shown via immunofluorescent stains. Overall, this study showed that SACs cause MDSC expansion from bone marrow cells and identified possible mediators to target as an additional strategy for treating chronic S. aureus infections.

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Observations on the binding and interaction of radioiodinated colony- stimulating factor with murine bone marrow cells in vivo

Blood ◽

10.1182/blood.v59.2.408.bloodjournal592408 ◽

1982 ◽

Vol 59 (2) ◽

pp. 408-420

Author(s):

G Pigoli ◽

A Waheed ◽

RK Shadduck

Keyword(s):

Bone Marrow ◽

Bone Marrow Cells ◽

Marrow Cell ◽

Cell Interaction ◽

Peritoneal Macrophages ◽

Colony Stimulating Factor ◽

Murine Bone Marrow ◽

Stimulating Factor ◽

Marrow Cells

Radioiodinated L-cell-derived colony-stimulating factor (CSF) was used to characterize the binding reaction to murine bone marrow cells. The major increment in cell-associated radioactivity occurred over 24 hr incubation at 37 degrees C, but virtually no binding was observed at 4 degrees C. The reaction was saturable with approximately 1 ng/ml of purified CSF. Unlabeled CSF prevented the binding, whereas a number of other hormones and proteins did not compete for CSF uptake. Further specificity studies showed virtually no binding to human bone marrow, which is unresponsive to this form of murine CSF. Minimal CSF uptake was noted with murine peritoneal macrophages, but virtually no binding was detected with thymic, lymph node, liver, or kidney cells. The marrow cell interaction with tracer appeared to require a new protein synthesis, as the binding was prevented by cycloheximide or puromycin. Preincubation of marrow cells in medium devoid of CSF increased the degree of binding after 1 hr exposure to the tracer. This suggests that CSF binding sites may be occupied or perhaps decreased in response to ambient levels of CSF in vivo. Approximately 70% of the bound radioactivity was detected in the cytoplasm at 24 hr. This material was partially degraded as judged by a decrease in molecular weight from approximately 62,000 to 2 peaks of approximately 32,000 and approximately 49,000, but 72% of the binding activity was retained. After plateau binding was achieved, greater than 80% of the radioactivity released into the medium was degraded into biologically inactive peptides with molecular weights less than 10,000. These findings suggest that the interaction of CSF with marrow cells is characterized by binding with subsequent internalization and metabolic degradation into portions of the molecule that are devoid of biologic activity.

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