C57BL/6 (popularly “C57 black 6”, or simply B6) is a black inbred strain established in 1921 by geneticist C. C. Little through continuous brother–sister mating of Abby Lathrop’s mice. In 1937 the line was split into C57BL/6 and C57BL/10; in 1947 The Jackson Laboratory designated its colony C57BL/6J, and 4 years later NIH derived the C57BL/6N substrain.
The two branches diverge genetically and phenotypically: C57BL/6J carries a loss-of-function mutation in the Nnt gene that impairs glucose metabolism and shows a distinct retinal arteriovenous branching pattern, whereas C57BL/6N harbors the Crb1rd8 allele that produces retinal degeneration and white fundus spots. Both substrains lack Ahl and consequently develop age-related hearing loss with high sensitivity to noise damage.
With a clear genetic background, stable breeding performance and robust constitution, C57BL/6 has become the first choice for oncology, genetics and immunology research, especially for transgenic or CRISPR model generation. It is the most widely used and fully commercialized mouse strain worldwide and was the first laboratory mouse to have its genome completely sequenced.
In previous lessons we described the use of clodronate liposomes to deplete macrophages in liver, lung, gut and brain. Today we summarize publications and protocols that employ clodronate liposomes specifically in C57BL/6 mice.
Literature 1
Article Source: PCSK9 Modulates Macrophage Polarization-Mediated Ventricular Remodeling after Myocardial Infarction (IF=3.6,Q2)
Macrophage Clearance Methods:
150 µL clodronate liposomes (5 mg mL⁻¹) were injected i.v. via the tail vein 24 h before and after coronary artery ligation; controls received PBS.
Results are shared:
Immunohistochemistry for F4/80 revealed a marked reduction of cardiac macrophages.
Literature 2
Article Source: AdMSC-derived exosomes alleviate acute lung injury via transferring mitochondrial component to improve homeostasis of alveolar macrophages (IF=13.3,Q1)
Macrophage Clearance Methods:
Wild-type C57BL/6 mice (8 weeks old) received 100 µL clodronate liposomes (Yeasen, Shanghai) intranasally to deplete alveolar macrophages.
Results are shared:
BAL cytology confirmed 90 % depletion of alveolar macrophages compared with PBS-treated controls.
Literature 3
Article Source: Differential role of tumor necrosis factor (TNF)-alpha receptors in the development of choroidal neovascularization (IF=4.7,Q1)
Macrophage Clearance Methods:
C57BL/6J (WT), Tnfrsf1a⁻/⁻ and Tnfrsf1b⁻/⁻ mice were given 200 µL clodronate liposomes i.v. via the tail vein 2 days before and immediately after laser photocoagulation. Macrophage clearance was assessed by F4/80 immunostaining.
Results are shared:
Depletion of circulating macrophages significantly reduced CNV area in WT and Tnfrsf1a⁻/⁻ mice. Choroidal flat-mounts from PBS-treated animals showed large CNV lesions with abundant F4/80⁺ infiltrates, whereas clodronate markedly diminished both macrophage recruitment and CNV formation. Similar reductions were observed in Tnfrsf1b⁻/⁻ mice.
Literature 4
Article Source: Roquin-1 Regulates Macrophage Immune Response and Participates in Hepatic Ischemia-Reperfusion Injury (IF=3.4,Q2)
Macrophage Clearance Methods:
Male wild-type C57BL/6 mice (6–8 weeks) received 400 µL clodronate liposomes i.p. To prevent opportunistic infections, animals were maintained on ampicillin (1 mg mL⁻¹) in drinking water until sacrifice. Resident peritoneal and Kupffer-cell depletion was verified by flow cytometry and immunohistochemistry 48 h later.
Results are shared:
Both immunohistochemistry (a) and flow cytometry (b) confirmed efficient hepatic-macrophage depletion. Co-immunofluorescence (c) showed Roquin-1 (green) is predominantly expressed in hepatic macrophages (red) (n = 6).
Product Recommendation
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Product name |
Item number |
Specification |
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40337ES08 |
5 mL |
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40337ES10 |
10 mL |
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40338ES08 |
5 mL |
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40338ES10 |
10 mL |
We provides a complete reagent portfolio for macrophage research—from cell isolation, in-vitro generation, and depletion-model construction to functional validation—helping you generate high-impact publications.Please visit the Yeasen’s website.