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Human Small Airway Epithelial Cells

Cat.No.: CSC-C4106X

Species: Human

Source: Lung; Airway

Cell Type: Epithelial Cell

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Cat.No.
CSC-C4106X
Description
Creative Bioarray's normal Human Airway Epithelial Cells, when grown in Creative Bioarray's LIBro Medium, provide an ideal serum-free culture model for the accurate studies of toxicity, cystic fibrosis, asthma, pathogenesis, pharmacology or airway wound healing. Creative Bioarray's HSAEC are cultured without retinoic acid and cryopreserved as primary cells to ensure the highest viability and plating efficiency. Our HSAEC are quality tested in LIBro SAE Medium to ensure optimal growth over a period of at least 15 population doublings at rates equal to or greater than other commercially available media.

Cell Features:
HBTEC are cryopreserved as primary cells. Cells are isolated from human bronchi/trachea and expanded once in culture vessels before being harvested for cryopreservation.
HSAEC are cryopreserved after primary cells are isolated from human lung tissue and expanded once in culture vessels before being harvested for cryopreservation.
Creative Bioarray's Human Airway Epithelial Cells are not exposed to retinoic acid during isolation or expansion.
Human Airway Epithelial Cells are extensively tested for quality and optimal performance.
Creative Bioarray guarantees performance and quality.
Species
Human
Source
Lung; Airway
Cell Type
Epithelial Cell
Disease
Normal
Storage and Shipping
Store in liquid nitrogen and ship in dry ice.
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.

The small airways are located at the interface between alveoli and conducting airways. Airway epithelial cells form a continuous lining within the airways. They play a unique role as a protective physical and functional barrier against external deleterious agents.

Human Small Airway Epithelial Cells (HSAEpC) are isolated from the distal portion of lung tissue in the bronchiole area of the respiratory tract. They participate in host defense by producing chemokines and expressing adhesion molecules, thereby regulating immune responses. They also produce liquids contributing to pulmonary fluid balance. Many airway diseases, such as asthma, bronchiolitis, chronic obstructive pulmonary disease, and cystic fibrosis, involve damage to the airway surface epithelium. The study of human SAEpC may help to identify new therapeutic options for preventing airway disorders. HSAEpC are also useful tools for establishing in vitro disease models for high-throughput and high-content screening.

Human 3D small airway model.

Fig. 1. In vitro human 3D small airway model (Song Huang, et al. 2017).

Nanoplastics Penetrate Human Bronchial Smooth Muscle and Small Airway Epithelial Cells and Affect Mitochondrial Metabolism

Micro- and nanoplastic particles, including common forms like polyethylene and polystyrene, have been identified as relevant pollutants, potentially causing health problems in living organisms. The mechanisms at the cellular level largely remain to be elucidated. This study aims to visualize nanoplastics in bronchial smooth muscle (BSMC) and small airway epithelial cells (SAEC), and to assess the impact on mitochondrial metabolism.

Healthy and asthmatic human BSMC and SAEC in vitro cultures were stimulated with polystyrene nanoplastics (PS-NPs) of 25 or 50 nm size, for 1 or 24 h. Live cell, label-free imaging by holotomography microscopy and mitochondrial respiration and glycolysis assessment were performed. Furthermore, 25 and 50 nm NPs were shown to penetrate SAEC, along with healthy and diseased BSMC, and they impaired bioenergetics and induce mitochondrial dysfunction compared to cells not treated with NPs, including changes in oxygen consumption rate and extracellular acidification rate.

Human small airway epithelial cells (SAEC) exposed to 25 or 50 nm polystyrene nanoplastics (PS-NPs) for durations of 1 or 24 h exhibited a statistically significant reduction in oxygen consumption rate (OCR) compared to the control group that was not treated with NPs.

Fig. 1. Human small airway epithelial cells (SAEC) have impaired bioenergetics and dysfunctional mitochondria following exposure to polystyrene nanoplastics (PS-NPs) of 25 nm and 50 nm in diameter for durations of 1 h and 24 h, compared to SAEC that were not exposed to NPs (Winiarska, Ewa, et al. 2024).

A Viral Assembly Inhibitor Blocks SARS-CoV-2 Replication in Airway Epithelial Cells

The ongoing evolution of SARS-CoV-2 to evade vaccines and therapeutics highlights the need for innovative therapies with high genetic barriers to resistance. Therefore, there is pronounced interest in identifying new pharmacological targets in the SARS-CoV-2 viral life cycle.

PAV-104, a small molecule identified through a cell-free protein synthesis and assembly screen, was recently shown to target host protein assembly machinery in a manner specific to viral assembly. This study investigated the capacity of PAV-104 to inhibit SARS-CoV-2 replication in human airway epithelial cells (AECs). Results showed that PAV-104 inhibits >99% of infection with diverse SARS-CoV-2 variants in immortalized AECs, and in primary human AECs cultured at the air-liquid interface (ALI) to represent the lung microenvironment in vivo. PAV-104 interacts with SARS-CoV-2 nucleocapsid (N) and interferes with its oligomerization, blocking particle assembly. Transcriptomic analysis reveals that PAV-104 reverses SARS-CoV-2 induction of the type-I interferon response and the maturation of nucleoprotein signaling pathway known to support coronavirus replication. PAV-104 is a promising therapeutic candidate for COVID-19 with a mechanism of action distinct from existing clinical management approaches.

Antiviral activity of PAV-104 against SARS-CoV-2 in primary airway epithelial cells, as determined by RT-qPCR.

Fig. 2. PAV-104 inhibits the replication of SARS-CoV-2 variants in human primary airway epithelial cells (Du, Li, et al. 2024).

PAV-104 treatment suppresses the IFN signaling and maturation of nucleoprotein gene expression pathways.

Fig. 3. Impact of SARS-CoV-2 infection and PAV-104 treatment on the transcriptome of primary AECs (Du, Li, et al. 2024).

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