C57BL/6 Mouse Primary Tracheal Epithelial Cells

Cat.No.: CSC-C4248X

Species: Mouse

Source: Trachea

Cell Type: Epithelial Cell

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Cat.No.
CSC-C4248X
Description
C57BL/6 Mouse Primary Tracheal Epithelial Cells from Creative Bioarray are isolated from tissue of pathogen-free laboratory mice. Mouse Primary Tracheal Epithelial Cells are grown in T25 tissue culture flasks pre-coated with gelatin-based coating solution for 0.5 hour and incubated in Creative Bioarray's Culture Complete Growth Medium for 3-7 days. Cells are detached from flasks and immediately cryo-preserved in vials. Each vial contains at least 1x10^6 cells per ml and is delivered frozen.
Mouse Primary Tracheal Epithelial Cells can be used in assays of cell to cell adhesion and migration. Standard biochemical procedures performed with epithelial cell cultures include RT-PCR, Western blotting, immunoprecipitation, immunofluorescent staining or immunofluorescent flow cytometry or generating cell derivatives for desired research applications.
Species
Mouse
Source
Trachea
Recommended Medium
Complete Epithelial Cell Medium
Cell Type
Epithelial Cell
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.

C57BL/6 Mouse Primary Tracheal Epithelial Cells are obtained directly from the trachea of the C57BL/6 mouse strain, a genetically well-characterized and commonly used inbred model in biomedical research. These cells make up the mucosal lining of the upper airway and are critical to the maintenance of respiratory homeostasis via mucociliary clearance and barrier protection.

When grown under adherent circumstances, these cells display a distinctive epithelial shape in culture, developing as a polarized monolayer of cobblestone-like cells. They are usually cultivated in a specialized basal medium supplemented with growth factors, hormones and serum to maintain their original phenotype. Routine maintenance is performed in a humidified atmosphere of 37 °C with 5% carbon dioxide. Subculturing is done using a moderate protease solution.

Given their physiological importance these cells are an invaluable model to research airway biology, ciliary function and host-pathogen interactions, in particular in the context of viral infections such as influenza. They are also widely employed in studies of inflammatory responses, toxicological assessment and pathophysiology of chronic respiratory disorders, providing a species-specific platform that supports human bronchial epithelial cell models.

L-24 Specifically Targets Airway Epithelial Cells and Promotes Inflammatory Responses and Remodeling Processes

Asthma is a disease of persistent inflammation and airway remodeling, yet current medications seldom restore structural damage. IL-24 has been implicated in neutrophilic asthma, although its significance in eosinophilic asthma is unknown. Wu's team used IL-24 knockout mice in OVA/HDM models to determine the role of IL-24 to pulmonary disease as a possible therapeutic target.

They developed an ex vivo tracheal epithelial cell culture mimicking in vivo circumstances that provides a biologically relevant platform to study airway disorders. IL-24 stimulation consistently increased amphiregulin production in primary tracheal epithelial cells (Fig. 1i, j) and generated different transcriptome changes as shown by PCA (Fig. 1k). Differential gene expression analysis revealed a total of 138 DEGs, including 61 upregulated and 77 downregulated (Fig. 1l).

Among the upregulated genes were S100a8, C3, Ccl2, Cxcl5, and Mmp3, which are known to enhance airway inflammation and remodeling in asthma (Fig. 1l). However, IL-24 repressed important barrier maintenance genes, including epithelial sodium channels (Scnn1a/b/g), anion transporters (Slc26a9) and Aqp4 (Fig. 1l). These data suggest that IL-24 exacerbates airway disease by concurrently inducing a pro-inflammatory milieu and impairing epithelial barrier integrity.

IL-24 targets airway epithelial cells and promotes inflammatory responses and remodeling processes.

Fig. 1. IL-24 targets airway epithelial cells and promotes inflammatory responses and remodeling processes (Wu Y R, Hsing C H, et al., 2025).

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