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Sp5 inverted confocal laser microscope

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The Leica SP5 inverted confocal laser microscope is a high-performance imaging system designed for live-cell and fixed-sample analysis. It features a compact and modular design, allowing for customization to meet specific research needs. The SP5 utilizes laser excitation and confocal detection to provide optical sectioning, enabling the acquisition of detailed, high-resolution images of biological specimens.

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Lab products found in correlation

Thp 1 human monocytic cells, by American Type Culture Collection (2 mentions) Anti eea1, by Thermo Fisher Scientific (2 mentions) B6.129 tlr2tm1kir j mice, by Jackson ImmunoResearch (2 mentions) Bx51 upright microscope, by Olympus (1 mentions) Dulbecco modified eagle medium (dmem), by Thermo Fisher Scientific (1 mentions)

Close spelling variants of this product

TCS SP5 inverted laser scanning confocal microscope SP5 inverted confocal laser scanning microscope Leica SP5 X MP Inverted Laser Scanning Confocal Microscope SP5 inverted confocal microscope SP5 laser confocal microscope Inverted Confocal SP5 Inverted SP5 microscope SP5 confocal microscope Inverted confocal microscope Laser confocal microscope

4 protocols using sp5 inverted confocal laser microscope

1

Confocal Imaging and 3D Reconstruction

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Confocal imaging was performed using a Leica SP5 inverted confocal laser microscope (Leica) and three-dimensional reconstructions were generated using ImageJ. Histology and in situ images were obtained using an Olympus BX51 upright microscope with an Olympus Microfire digital camera. In all experiments, either arm II or III was visualized.
Nödl M.T., Fossati S.M., Domingues P., Sánchez F.J, & Zullo L. (2015). The making of an octopus arm. EvoDevo, 6, 19.
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2

FRAP Analysis of Cellular Dynamics

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FRAP experiments and analysis were performed as described before (Scotter et al, 2014 (link)) in a Leica SP5 inverted confocal laser microscope using 63X objective (NA 1.4). Cells were plated on 24‐well plates and cultured with phenol red‐free DMEM (Gibco, 31053028).
Pérez‐Berlanga M., Wiersma V.I., Zbinden A., De Vos L., Wagner U., Foglieni C., Mallona I., Betz K.M., Cléry A., Weber J., Guo Z., Rigort R., de Rossi P., Manglunia R., Tantardini E., Sahadevan S., Stach O., Hruska‐Plochan M., Allain F.H., Paganetti P, & Polymenidou M. (2023). Loss of TDP‐43 oligomerization or RNA binding elicits distinct aggregation patterns. The EMBO Journal, 42(17), e111719.
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3

Macrophage Differentiation and Rhinovirus Infection

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To generate bone marrow-derived macrophages, mouse bone marrow monocytes were isolated from C C57BL/6J and TLR2−/− (B6.129-Tlr2tm1Kir/J) mice (Jackson Laboratories) and cultured in L929 medium, a source of macrophage colony-stimulating factor, for 7 days 49 (link). Human primary peripheral blood mononuclear cells (PBMC; Precision for Medicine, Frederick, MD) were cultured in RPMI-1640 media supplemented with 20ng/mL of recombinant human M-CSF. THP-1 human monocytic cells (ATCC) were differentiated with 5 ng/ml of phorbol 12-myristate 13-acetate as described50 . Cells were infected with RV-A1B and RV-C15 at a multiplicity of infection (MOI) of 1.0 at 33°C. To study virus entry, human THP-1-derived macrophages and mouse bone marrow-derived macrophages were incubated with RV-A1B or RV-C15 for 1 hour and washed three times with PBS. Viral RNA and CDHR3 mRNA expression were quantified by qPCR (see below) and the presence of RV-C was examined by Western blot and immunofluorescence using anti-EV-D68 vp3. Late endosomes were visualized with anti-EEA1 (Invitrogen, Carlsbad, CA). Images were visualized using a Leica SP5 inverted laser confocal microscope (Buffalo Grove, IL).
Han M., Ishikawa T., Stroupe C.C., Breckenridge H.A., Bentley J.K, & Hershenson M.B. (2021). Deficient inflammasome activation permits an exaggerated asthma phenotype in rhinovirus C-infected immature mice. Mucosal immunology, 14(6), 1369-1380.
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4

Macrophage Differentiation and Rhinovirus Infection

Cited 1 time
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To generate bone marrow-derived macrophages, mouse bone marrow monocytes were isolated from C C57BL/6J and TLR2−/− (B6.129-Tlr2tm1Kir/J) mice (Jackson Laboratories) and cultured in L929 medium, a source of macrophage colony-stimulating factor, for 7 days 49 (link). Human primary peripheral blood mononuclear cells (PBMC; Precision for Medicine, Frederick, MD) were cultured in RPMI-1640 media supplemented with 20ng/mL of recombinant human M-CSF. THP-1 human monocytic cells (ATCC) were differentiated with 5 ng/ml of phorbol 12-myristate 13-acetate as described50 . Cells were infected with RV-A1B and RV-C15 at a multiplicity of infection (MOI) of 1.0 at 33°C. To study virus entry, human THP-1-derived macrophages and mouse bone marrow-derived macrophages were incubated with RV-A1B or RV-C15 for 1 hour and washed three times with PBS. Viral RNA and CDHR3 mRNA expression were quantified by qPCR (see below) and the presence of RV-C was examined by Western blot and immunofluorescence using anti-EV-D68 vp3. Late endosomes were visualized with anti-EEA1 (Invitrogen, Carlsbad, CA). Images were visualized using a Leica SP5 inverted laser confocal microscope (Buffalo Grove, IL).
Han M., Ishikawa T., Stroupe C.C., Breckenridge H.A., Bentley J.K, & Hershenson M.B. (2021). Deficient inflammasome activation permits an exaggerated asthma phenotype in rhinovirus C-infected immature mice. Mucosal immunology, 14(6), 1369-1380.
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