Immortalized Human Small Airway Epithelial Cells-SV40

Immortalized Human Small Airway Epithelial Cells-SV40

Cat.No.: CSC-I9068L

Species: Homo sapiens

Source: Lung

Morphology: Polygonal

Culture Properties: Adherent

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Cat.No.
CSC-I9068L
Description
The small airways epithelial cells form a continuous lining to the airways play a unique role as a protective physical and functional barrier to external deleterious agents. These cells function in the regulation of immune responses by contributing to host defense through chemokine production, adhesion molecule expression, and possibly antigen presentation via HLA-DR expression. These cells provide an ideal model for the studies of toxicity, cystic fibrosis, asthma, pathogenesis, pharmacology or airway wound healing.
Species
Homo sapiens
Source
Lung
Culture Properties
Adherent
Morphology
Polygonal
Immortalization Method
Serial passaging and transduction with recombinant lentiviruses carrying SV40 Large T antigen
Markers
Cytokeratin
Application
For Research Use Only
Storage
Directly and immediately transfer cells from dry ice to liquid nitrogen upon receiving and keep the cells in liquid nitrogen until cell culture needed for experiments.

Note: Never can cells be kept at -20 °C.
Shipping
Dry Ice.
Recommended Products
CSC-C4106X Human Small Airway Epithelial Cells
CIK-HT003 HT® Lenti-SV40T Immortalization Kit
Quality Control
Real Time PCR was used to quantify SV40 gene expression in immortalized cell line.
BioSafety Level
II
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.

Immortalized human small airway epithelial cells-SV40 (HSAEC/SV40) are generated by introducing the SV40 large T antigen into primary human small airway epithelial cells. This confers indefinite proliferative capacity while preserving core epithelial features, including pan-cytokeratin, E-cadherin, ZO-1, and occludin. Depending on the line, they may retain club cell-associated markers such as SCGB1A1/CC10 and mucus-related proteins. Functionally, they form barrier-competent monolayers and respond to inflammatory and microbial stimuli via Toll-like receptors, secreting cytokines and chemokines such as IL-6, IL-8, and TNF-α.

Compared with primary HSAECs, HSAEC/SV40 offer a continuous, scalable, and cost-effective source with high batch-to-batch consistency and reduced donor variability. This enables reproducible high-throughput screening, long-term culture, and gene perturbation using siRNA or CRISPR. They are widely used to model small airway epithelial injury and inflammation in COPD, asthma, cystic fibrosis, and respiratory viral infections, including RSV, influenza, and SARS-CoV-2. They also support inhalation toxicology, drug transport, and biocompatibility testing.

PIWIL4 Regulates Gene Expression and piRNA Levels in RSV-Infected Airway Epithelial Cells

Respiratory syncytial virus (RSV) causes acute lower respiratory tract infection in young children, the elderly, and immunocompromised hosts, and no RSV vaccine or therapy exists for infants, beyond prophylaxis. PIWI-interacting RNAs (piRNAs), small non-coding RNAs acting through P element-induced wimpy testis (Piwi) proteins, remain largely unexplored. This study characterized PIWIL4 expressions and function during RSV infection or poly(I:C) stimulation, a proxy of viral infection. PIWIL4 was expressed in primary and immortalized small airway epithelial cells following RSV infection. While PIWIL4 knockdown did not affect RSV replication, it decreased cytokine and growth factor secretion, altered gene and piRNA expression, and modulated pathways involved in cytokine production, metabolism, and airway remodeling. Limited overlap between piRNA targets and transcriptomic changes suggests PIWIL4 regulates airway epithelial cell responses partly independently of piRNAs. This study positions PIWIL4 as a key regulator of airway epithelial cell responses to viral infections.

Changes in PIWIL4 expression and cellular localization in airway epithelial cells following RSV infection.
Fig. 1. PIWIL4 mRNA and protein expression in immortalized small airway epithelial cells following RSV infection and poly(I:C) treatment (Corsello, Tiziana, et al., 2026).
PIWIL4 deficiency alters the pro-inflammatory cytokine and growth factor profile during RSV infection.
Fig. 2. Effect of PIWIL4 silencing on immune mediator production in RSV-infected iSAE cells (Corsello, Tiziana, et al., 2026).

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