C57BL/6 (commonly known as “C57 Black 6,” abbreviated as B6) is a black inbred mouse strain established in 1921 by geneticist C.C. Little through continuous brother-sister mating of mice from Abby Lathrop’s colony. In 1937, this strain was further subdivided into two branches: C57BL/6 and C57BL/10. In 1947, The Jackson Laboratory designated its stock as C57BL/6J; five years later, the NIH derived another substrain, C57BL/6N, from this line.
These two major substrains have diverged at both the genomic and phenotypic levels:
- C57BL/6J carries a mutation in the Nnt gene, resulting in impaired glucose metabolism, and exhibits significantly different retinal vascular branching patterns compared to C57BL/6N.
- C57BL/6N harbors the Crb1rd8 allele, which causes retinal degeneration and white fundus spots.
Both substrains lack the Ahl allele, leading to age-related hearing loss and heightened susceptibility to noise-induced damage.
Thanks to their well-defined genetic background, stable reproduction, and robust health, C57BL/6 mice have become the preferred model in cancer, genetics, and immunology research—particularly for generating transgenic or gene-edited models. It is currently the most widely used and commercially available mouse strain worldwide and was the first laboratory mouse to have its whole genome sequenced.
Previously, we introduced applications of macrophage-depleting agents (Clodronate Liposomes) in depleting macrophages in the liver, lung, intestine, brain, and peripheral blood. Today, we share relevant literature and protocols on using Clodronate Liposomes to deplete splenic macrophages.
Representative Literature and Protocols
Literature 1
Source: Pharmacological macrophage inhibition decreases metastasis formation in a genetic model of pancreatic cancer
Impact Factor: 25.8 (Q1)
Macrophage Depletion Protocol: In a long-term treatment regimen, KPC mice received intraperitoneal injections of clodronate liposomes twice weekly from 8 weeks (P56) to 20 weeks of age (P140). The dosage was 1.4 mg per 20 g body weight, with PBS liposomes administered as controls.
Key Findings：
After short-term (2-week) treatment, flow cytometry analysis revealed reductions of:
- 48% in pancreatic CD68⁺ cells
- 56% in splenic CD68⁺ cells
- 73% in bone marrow CD68⁺ cells
Further gating showed a significant decrease in CD11b⁺Gr1⁻ macrophages/monocytes, while CD11b⁺Gr1⁺ myeloid-derived suppressor cells (MDSCs) were unaffected, demonstrating selective macrophage depletion.
Literature 2
Source: Macrophage autophagy protects against acute kidney injury by inhibiting renal inflammation through the degradation of TARM1
Impact Factor: 14.3 (Q1)
Macrophage Depletion Protocol: Prior to macrophage transplantation, recipient mice were injected intravenously with clodronate liposomes at 0.1 mL per 10 g body weight to deplete circulating macrophages.
Key Findings：
Clodronate-induced macrophage depletion significantly protected SA-AKI mice from renal injury and inflammation, reinforcing the central role of macrophages as immune drivers in acute kidney injury.
Literature 3
Source: Elimination of macrophages reduces glutaraldehyde-fixed porcine heart valve degeneration in a mouse subdermal model
Impact Factor: 2.3 (Q3)
Macrophage Depletion Protocol: Male C57BL/6 mice received clodronate liposome injections one day prior to surgery, followed by additional doses on post-implantation days 2, 5, 8, and 11.
Key Findings：
Seven days after treatment, ~80% depletion of splenic F4/80⁺ macrophages was observed compared with controls, confirming effective macrophage removal. Treated mice showed no signs of infection, appetite loss, or reduced activity. Immunohistochemical analysis at day 28 further confirmed sustained suppression of F4/80⁺ macrophage infiltration in the spleen.
Literature 4
Source: Phagocyte depletion inhibits AA amyloid accumulation in AEF-induced huIL-6 transgenic mice
Impact Factor: 7.4 (Q1)
Macrophage Depletion Protocol: Transgenic huIL-6 mice received intravenous injections of 0.1 mL liposome suspension at defined time points.
Key Findings:
Clodronate liposomes induced a selective and transient loss of splenic phagocytes. Three days post-treatment, F4/80⁺ macrophages in the spleen and liver were almost completely absent, with partial recovery observed by day 5, highlighting the reversible and controllable nature of clodronate-mediated depletion.
Complete Solutions for Macrophage Research
Yeasen Biotechnology offers a comprehensive portfolio of reagents for macrophage research—covering every stage from macrophage isolation and polarization, to in vivo depletion model establishment, mechanistic functional studies, and immunological validation assays. Our integrated solutions help researchers accelerate discovery, improve reproducibility, and support publication in high-impact journals.
Related Product
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Name |
Cat. No. |
Size |
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40337ES08/10 |
5 mL/10 mL |
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40338ES08/10 |
5 mL/10 mL |