BALB/c Mouse Peritoneal Macrophages-Thioglycollate-elicited

Cat.No.: CSC-C4334X

Species: Mouse

Source: Peritoneal Cavity

Cell Type: Macrophage

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Cat.No.
CSC-C4334X
Description
Mouse Peritoneal Macrophages are derived from the thioglycollate-elicited peritoneal cavity of pathogen-free laboratory adult mice. Mouse Peritoneal Macrophages are negative for bacteria, yeast, fungi, and mycoplasma. Each vial contains at least 8 x10^6 cells and is delivered frozen.
Cells can be expanded on a multiwell culture plate ready for experiments under the cell culture conditions specified by Creative Bioarray. Repeated freezing and thawing of cells is not recommended.
Mouse Peritoneal Macrophages are tested for expression of markers using antibodies, CD11b by flow cytometry.
Standard biochemical procedures performed with cell cultures include RT-PCR, Western blotting, immunoprecipitation, immunofluorescent staining, flow cytometry or generating cell derivatives for desired research applications.
Species
Mouse
Source
Peritoneal Cavity
Recommended Medium
Complete Macrophage Medium
Cell Type
Macrophage
Disease
Normal
Storage and Shipping
Creative Bioarray will ship frozen cells on dry ice. On receipt, immediately transfer frozen cells to liquid nitrogen (-180 °C) until ready for experimental use. Live-cell shipment is also available on request.
Citation Guidance
If you use this products in your scientific publication, it should be cited in the publication as: Creative Bioarray cat no. If your paper has been published, please click here to submit the PubMed ID of your paper to get a coupon.

BALB/c mouse peritoneal macrophages elicited with thioglycollate represent a widely used primary macrophage model for studying innate immunity and inflammation. Following intraperitoneal injection of sterile thioglycollate medium, a localized sterile inflammatory response is induced, leading to the rapid recruitment of monocytes from the blood into the peritoneal cavity. These recruited cells subsequently differentiate into activated macrophages, which can be harvested by peritoneal lavage after 3-5 days.

The principal advantage of thioglycollate-elicited peritoneal macrophages lies in their high yield and functional activity. Compared to resident peritoneal macrophages, which are relatively quiescent and low in number, thioglycollate elicitation typically yields 10-20 million cells per mouse with enhanced phagocytic capacity, microbicidal activity, and responsiveness to toll-like receptor (TLR) ligands. These cells express elevated levels of activation markers (e.g., CD80, CD86, MHC class II) and secrete robust amounts of pro-inflammatory cytokines (e.g., TNF-α, IL-6, IL-1β) upon stimulation.

Moreover, the BALB/c background is well-characterized, providing experimental consistency and comparability across studies. These macrophages are highly amenable to ex vivo assays, including flow cytometry, immunofluorescence, phagocytosis, and intracellular pathogen killing. Their ease of isolation, reproducible phenotype, and functional maturity make them an indispensable tool for immunologists investigating host defense, vaccine adjuvancy, drug screening, and inflammatory disease mechanisms.

MiR-146b-5p Inhibits Candida Albicans-Induced Inflammatory Response Through Targeting HMGB1 in Mouse Primary Peritoneal Macrophages

Candida albicans (C. albicans) is one of the most common pathogens associated with deep fungal infection, which represents a serious threat to human health. Although high mobility group box 1 (HMGB1) plays a key role in C. albicans infection, its mechanism is unclear. Currently, a large number of studies on miRNA-mediated regulation of HMGB1 have focused on bacterial sepsis, whereas studies on C. albicans sepsis are lacking. Therefore, our purpose is to study miRNAs that regulate HMGB1, which is crucial in C. albicans sepsis.

In this study, mouse primary peritoneal macrophages (MPMs) infected with C. albicans were used to elucidate the changes in the miRNA expression profile. Through screening and verification, mmu-miR-146b-5p was identified as a miRNA targeting HMGB1 for the first time. We further investigated the regulation of mmu-miR-146b-5p on HMGB1, inflammatory mediators, and the NF-κB signaling pathway during C. albicans infection to provide a potential target for the treatment of C. albicans infection. The results demonstrate that mmu-miR-146b-5p directly and negatively regulate the expression and translocation of HMGB1, inhibit the expression of inflammatory mediators, and might participate in the NF-κB signaling pathway in a HMGB1-dependent manner under C. albicans infection.

Mmu-miR-146b-5p inhibits the translocation of HMGB1 in MPMs.

Fig. 1. HMGB1 nuclear and cytoplasm translocation was inhibited by mmu-miR-146b-5p in C. albicans-stimulated MPMs (Cheng, Jing, et al., 2025).

Mmu-miR-146b-5p modulates C. albicans-induced inflammatory mediators.

Fig. 2. The expression of inflammatory mediators might be inhibited by mmu-miR-146b-5p in C. albicans-induced MPMs (Cheng, Jing, et al., 2025).

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