PneumaCult™-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 PneumaCult™-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.
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Animal Component-Free Cell Dissociation KitDissociation kit for human stem and progenitor cells
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Hydrocortisone Stock SolutionCell culture supplement
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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 (61)
Blocking AGEs reduces airway epithelial viral susceptibility in diabetes-exacerbated COPD.
EMBO molecular medicine 2026 Sep
Abstract
Although diabetic complications are well-established in multiple organs, their impact on the respiratory system remains unclear. Clinical evidence indicates accelerated chronic obstructive pulmonary disease (COPD) progression in individuals with diabetes, yet the underlying mechanisms are poorly defined. Using single-cell RNA sequencing of airway epithelium, we identified distinct transcriptional alterations in COPD patients with or without diabetes, particularly in host-defense pathways related to viral infection, which is a key driver of COPD exacerbations. Functionally, hyperglycemia enhanced influenza virus susceptibility in both COPD-derived epithelial cells and COPD mice with diabetes, indicating compromised airway defense. We further demonstrated that hyperglycemia promotes advanced glycation end products (AGEs) accumulation in airway epithelium, with AGEs levels correlating with infection severity. Pharmacological inhibition of AGEs formation with aminoguanidine significantly reduced viral load both in vitro and in vivo. Mechanistically, AGEs activate p38/ERK/IKK proinflammatory signaling via RAGE and MD2 receptors, leading to epithelial injury and heightened viral susceptibility. Our findings reveal a hyperglycemia-AGEs-RAGE/MD2 axis that increases viral susceptibility in COPD, highlighting AGEs targeting as a promising therapeutic strategy for COPD patients with diabetes.
ATP/P2X7 signaling as a potential predictive biomarker for early recurrence of nasal polyps: Correlation with inflammasome activation and epithelial barrier dysfunction.
The World Allergy Organization journal 2026 Sep
Abstract
BACKGROUND: Chronic rhinosinusitis with nasal polyps (CRSwNP) is characterized by pronounced epithelial remodeling and barrier dysfunction, contributing to a high rate of postoperative recurrence. However, molecular mechanisms associated with early recurrence remain poorly understood. METHODS: We performed paired proteomic profiling of nasal polyp tissues obtained from the same patients before initial surgery and at the time of recurrence (discovery cohort) to identify recurrence-associated proteins. Candidate proteins were validated in an independent cohort, and their association with recurrence risk was assessed by receiver operating characteristic (ROC) curve and Kaplan-Meier analyses. The expression and cellular localization of the identified candidate were further characterized by immunofluorescence. Mechanistic investigations were conducted in primary human nasal epithelial cells using ATP stimulation and specific pharmacological inhibitors. RESULTS: Paired proteomic analysis identified P2X7, PDE4D, and JADE2 as the top 3 upregulated proteins in recurrent tissues. Among these, only P2X7 was consistently elevated in the validation cohort and predominantly localized to the nasal epithelium (P < 0.01). ROC curve analysis indicated that tissue P2X7 level might serve as a potential predictive marker for postoperative recurrence of CRSwNP. (AUC = 0.678, P = 0.022). Kaplan-Meier analysis further showed that the risk of recurrence was significantly higher in the high P2X7 expression group (HR = 2.323, P = 0.015). Recurrent tissues exhibited elevated levels of NLRP3 and IL-1β, reduced expression of epithelial barrier markers occludin and E-cadherin, accompanied by increased extracellular ATP concentrations. In vitro, ATP stimulation upregulated P2X7 expression, induced NLRP3 and cleaved IL-1β, and downregulated occludin and E-cadherin. Notably, these effects were reversed by a P2X7-specific inhibitor (A-438079). CONCLUSION: Paired proteomic profiling revealed distinct protein expression profiles between pre- and post-recurrence nasal polyps, with P2X7 serving as a promising predictive biomarker for early recurrence. Mechanistically, the ATP/P2X7 axis may drive disease recurrence by potentially promoting inflammasome activation and epithelial barrier disruption.
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.
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Want even better HAEC expansion rates and differentiation potential? Use PneumaCult™-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 STEMCELL, REFER TO WWW.STEMCELL.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 STEMCELL, REFER TO WWW.STEMCELL.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 www.P65Warnings.ca.gov
