PneumaCultâ„¢-Ex Plus Medium
Serum- and BPE-free medium for expansion of primary human airway epithelial cells
Want even better HAEC expansion rates and differentiation potential? Use PneumaCultâ„¢-NGEx Medium, our most advanced and optimized expansion medium, to achieve up to 250x more cells in just three weeks.
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Products for Your Protocol
To see all required products for your protocol, please consult the
Protocols and Documentation.
- Animal Component-Free Cell Dissociation Kit
Dissociation kit for human stem and progenitor cells
- Hydrocortisone Stock Solution
Cell culture supplement
- D-PBS (Without Ca++ and Mg++)
Dulbecco’s phosphate-buffered saline without calcium and magnesium
Overview
Data Figures
Protocols and Documentation
Find supporting information and directions for use in the Product Information Sheet or explore additional protocols below.
Applications
This product is designed for use in the following research area(s) as part of the highlighted workflow stage(s). Explore these workflows to learn more about the other products we offer to support each research area.
Resources and Publications
Educational Materials (18)
Publications (58)
Nuclear protein 1 is a cell death regulator in primary human airway epithelial cells and reduced in idiopathic pulmonary fibrosis
Scientific Reports 2026 May
Abstract
The airway epithelium is the first site of injury from cigarette smoke (CS), a major risk factor for chronic lung disease including idiopathic pulmonary fibrosis (IPF). Here, we report the first intracellular proteomic analysis of CS exposure in fully differentiated primary human bronchial epithelial cells (phBECs). Following pathway enrichment analysis, we identified nuclear protein 1 (NUPR1) as a candidate regulator of epithelial stress responses. In contrast to the prediction by pathway enrichment analysis, NUPR1 activity was not altered by CS in vitro. Nevertheless, inhibition of its nuclear translocation using ZZW-115 revealed a cytoprotective and anti-apoptotic role in phBECs, as demonstrated by increased apoptosis and impaired epithelial integrity. NUPR1 expression was markedly reduced in IPF whole lung tissue and bronchial epithelium. IPF-derived basal cells differentiated into an epithelium exhibiting fewer ciliated and more secretory cells which exhibited significantly higher sensitivity to NUPR1 inhibition. Our findings underscore cell type- and tissue-specific variation in NUPR1-dependent pathways. Collectively, this study positions NUPR1 as a context-dependent epithelial stress regulator whose loss may contribute to epithelial vulnerability in IPF.Supplementary InformationThe online version contains supplementary material available at 10.1038/s41598-026-51510-1.
CRSwNP-derived cells retain native disease-relevant characteristics in vitro
Journal of Inflammation (London, England) 2026 Mar
Abstract
Objective and designChronic rhinosinusitis (CRS) is a heterogeneous inflammatory disease of the paranasal sinuses, which is divided into CRS with nasal polyps (CRSwNP) and CRS without nasal polyps (CRSsNP). CRSwNP is typically caused by type 2 inflammation, which is characterized by elevated IL-4 and IL-13 levels, impairment of the epithelial barrier, and tissue remodeling. While the involvement of immune cells is well known, it remains unclear to what extent structural cells intrinsically maintain disease-specific functional programs. The aim of this study was to determine whether epithelial cells and fibroblasts derived from CRSwNP and CRSsNP differ in their barrier properties, inflammatory reactivity, and type 2-associated functional characteristics.MethodsAir–liquid interface (ALI) epithelial cultures and primary fibroblast cultures were generated from CRSwNP and CRSsNP tissue. Epithelial barrier integrity was assessed by transepithelial electrical resistance (TEER), and inflammatory responses to TLR stimulation were analyzed by qRT-PCR. Fibroblast migration was evaluated using scratch assays. Cellular responses to IL-4/IL-13 with or without Dupilumab were quantified by qRT-PCR.ResultsCRSwNP-derived epithelial cells exhibited delayed tight junction formation and impaired differentiation compared to CRSsNP cells. Poly(I:C) stimulation induced stronger expression of Th2-associated cytokines in CRSwNP cultures. CRSwNP fibroblasts showed reduced migratory capacity and a heightened induction of Th2 cytokines and extracellular matrix genes following IL-4/IL-13 stimulation relative to CRSsNP fibroblasts.ConclusionEpithelial cells and fibroblasts derived from CRSwNP retain disease-associated type 2 characteristics in vitro, indicating persistent disease-aligned programmed functional alterations of the polyp microenvironment. In contrast, CRSsNP-derived cells lacked comparable enhanced type 2 responsiveness. These findings support CRSwNP as a distinct, self-sustaining inflammatory endotype and underscore the value of patient-derived models for investigating disease mechanisms and targeted therapies.Supplementary InformationThe online version contains supplementary material available at 10.1186/s12950-026-00497-7.
Myeloperoxidase impairs mucociliary transport on human airway epithelium.
Disease models & mechanisms 2026 Jun
Abstract
Dampening neutrophil-driven inflammation in the airways remains a challenge in treating cystic fibrosis (CF) lung disease. Myeloperoxidase (MPO) is a neutrophilic enzyme that produces reactive oxygen species and is highly concentrated in CF airways. Greater MPO concentrations have previously been correlated with increased mucus plugging in bronchiectasis, suggesting that MPO could impair mucociliary transport. As such, we evaluated the impact of MPO treatment on barrier integrity, mucin production, mucus viscoelasticity and mucociliary transport in fully differentiated human airway epithelial cultures at ionic conditions reflective of healthy and CF-affected airways. Using live-cell imaging and particle velocimetry, we found that MPO inhibits mucociliary transport in vitro at CF-like and normal airway conditions. The impairment of mucus clearance by MPO was similar to that by neutrophil elastase, another neutrophilic granular enzyme that damages the host tissues and impairs airway clearance. We also found that subsequent treatment with the reducing agent, N-acetyl cysteine, could alleviate MPO-mediated mucociliary dysfunction through disulfide bond cleavage. These findings identify MPO as a therapeutic target to resolve deficits in airway clearance function in CF and related muco-obstructive lung diseases.
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Want even better HAEC expansion rates and differentiation potential? Use PneumaCultâ„¢-NGEx Medium, our most advanced and optimized expansion medium, to achieve up to 250x more cells in just three weeks.
Legal Statement:
This product was developed under a license to intellectual property owned or controlled by Propagenix, Inc. This product is sold for research use only (which includes pre-clinical research) under a non-transferable, limited-use license. Purchase of this product does not include the right to sell, use or otherwise transfer this product for commercial purposes or clinical use. Purchasers wishing to use the product for purposes other than research use should contact Propagenix, Inc. (www.propagenix.com/about#contact-us).
This product was developed under a license to intellectual property owned or controlled by Propagenix, Inc. This product is sold for research use only (which includes pre-clinical research) under a non-transferable, limited-use license. Purchase of this product does not include the right to sell, use or otherwise transfer this product for commercial purposes or clinical use. Purchasers wishing to use the product for purposes other than research use should contact Propagenix, Inc. (www.propagenix.com/about#contact-us).
Quality Statement:
PRODUCTS ARE FOR RESEARCH USE ONLY AND NOT INTENDED FOR HUMAN OR ANIMAL DIAGNOSTIC OR THERAPEUTIC USES UNLESS OTHERWISE STATED. FOR ADDITIONAL INFORMATION ON QUALITY AT º£½ÇÆƽâ°æ, REFER TO WWW.º£½ÇÆƽâ°æ.COM/COMPLIANCE.
PRODUCTS ARE FOR RESEARCH USE ONLY AND NOT INTENDED FOR HUMAN OR ANIMAL DIAGNOSTIC OR THERAPEUTIC USES UNLESS OTHERWISE STATED. FOR ADDITIONAL INFORMATION ON QUALITY AT º£½ÇÆƽâ°æ, REFER TO WWW.º£½ÇÆƽâ°æ.COM/COMPLIANCE.
Safety Statement:
CA WARNING: This product can expose you to Progesterone which is known to the State of California to cause cancer. For more information go to
