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
More Information
| 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 |
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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 (38)
Evolutionary loss of an antibiotic efflux pump increases Pseudomonas aeruginosa quorum sensing mediated virulence in vivo
Nature Communications 2025 Sep
Abstract
Antibiotic resistance is a threat to human health, yet recent work highlights how loss of resistance may drive pathogenesis in some bacteria. In two recent studies, we found that β-lactam antibiotics and nutrient stresses faced during infection selected for genetic inactivation of the Pseudomonas aeruginosa antibiotic efflux pump mexEFoprN . Unexpectedly, efflux pump mutations increased P. aeruginosa virulence during infection; however, neither the prevalence of mexEFoprN inactivating mutations in real human infections, nor the mechanisms driving increased virulence of efflux pump mutants are known. We hypothesized that human infection would select for virulence enhancing mutations. Using genome sequencing of clinical isolates, we show that mexEFoprN efflux pump inactivating mutations are enriched in P. aeruginosa isolates from cystic fibrosis infections relative to isolates from acute respiratory infections. Combining RNA-seq, metabolomics, genetic approaches, and infection models we show that efflux pump mutants have elevated quorum sensing driven expression of elastase and rhamnolipids which increase P. aeruginosa virulence during acute and chronic infections. Restoration of the efflux pump in a representative respiratory isolate and the notorious cystic fibrosis Liverpool epidemic strain reduced their virulence. These findings suggest that mutations inactivating antibiotic resistance mechanisms could lead to greater patient mortality and morbidity. Subject terms: Antimicrobial resistance, Pathogens, Bacteriology, Molecular evolution
Inhibition of LOXL2 Suppresses Nasal Mucosal Inflammation and Remodeling in Allergic Rhinitis
Journal of Asthma and Allergy 2025 Sep
Abstract
Tissue remodeling is a key feature of allergic rhinitis (AR), but its underlying molecular mechanisms remain unclear. Lysyl oxidase-like 2 (LOXL2), a regulator of tissue remodeling, has not been studied in AR. Proteomic analysis was performed on nasal mucosal tissues from 8 AR patients and 8 healthy controls (HCs) to identify differentially expressed proteins (DEPs). The top three upregulated DEPs and their association with tissue remodeling markers were validated by immunofluorescence, Western blot, and RT-qPCR in an independent cohort of 30 AR patients and 30 HCs. In vitro, human nasal epithelial cells (HNECs) were treated with IL-4, and the effects of candidate protein inhibitors on remodeling were assessed. An AR mouse model was used to evaluate the impact of these inhibitors on nasal inflammation and remodeling. Proteomic analysis revealed a disease-specific protein expression profile in the nasal mucosa of AR patients, with the top three upregulated proteins being LOXL2, TGF-β1, and TIRAP. Tissue validation showed that LOXL2 was significantly upregulated in the nasal mucosa of AR patients compared to HCs and was significantly correlated with EMT markers (TGF-β1, α-SMA, and E-cadherin). In vitro, IL-4 stimulation significantly upregulated LOXL2, TGF-β1, and α-SMA, while downregulating E-cadherin in a dose-dependent manner in human nasal epithelial cells. These effects were reversed by inhibition of LOXL2. Further investigations demonstrated that LOXL2 promotes tissue remodeling through activation of the TGF-β1/Smad signaling pathway. In the AR mouse model, LOXL2 inhibitors significantly reduced nasal mucosal inflammation and tissue remodeling. Our proteomic analysis suggests that LOXL2 may be involved in the pathological remodeling processes of AR, potentially through modulation of the TGF-β1/Smad signaling pathway. These findings provide preliminary evidence that LOXL2 could serve as a candidate biomarker and a possible therapeutic target in AR, warranting further investigation.
Influenza-induced microRNA-155 expression is altered in extracellular vesicles derived from the COPD epithelium
Frontiers in Cellular and Infection Microbiology 2025 May
Abstract
Influenza virus particularly affects those with chronic lung conditions such as Chronic Obstructive Pulmonary Disease (COPD). Airway epithelial cells are the first line of defense and primary target of influenza infection and release extracellular vesicles (EVs). EVs can transfer of biological molecules such as microRNAs (miRNAs) that can modulate the immune response to viruses through control of the innate and adaptive immune systems. The aim of this work was to profile the EV miRNAs released from bronchial epithelial cells in response to influenza infection and discover if EV miRNA expression was altered in COPD. Influenza infection of air-liquid interface (ALI) differentiated BCi-NS1.1 epithelial cells were characterized by analyzing the expression of antiviral genes, cell barrier permeability and cell death. EVs were isolated by filtration and size exclusion chromatography from the apical surface wash of ALI cultured bronchial epithelial cells. The EV miRNA cargo was sequenced and reads mapped to miRBase. The BCi sequencing results were further investigated by RT-qPCR and by using healthy and COPD primary epithelial cells. Infection of ALI cultured BCi cells with IAV at 3.6 x 10 6 IU/ml for 24 h led to significant upregulation of anti-viral genes without high levels of cell death. EV release from ALI-cultured BCi cells was confirmed using electron microscopy and detection of known tetraspanin EV markers using western blot and the ExoView R100 platform. Differential expression analyses identified 5 miRNA that had a fold change of >0.6: miR-155-5p, miR-122-5p, miR-378a-3p, miR-7-5p and miR-146a-5p (FDR<0.05). Differences between EV, non-EV and cellular levels of these miRNA were detected. Primary epithelial cell release of EV and their miRNA cargo was similar to that observed for BCi. Intriguingly, miR-155 expression was decreased in EVs derived from COPD patients compared to EVs from control samples. Epithelial EV miRNA release may be a key mechanism in modulating the response to IAV in the lungs. Furthermore, changes in EV miRNA expression may play a dysfunctional role in influenza-induced exacerbations of COPD. However, further work to fully characterize the function of EV miRNA in response to IAV in both health and COPD is required.
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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 şŁ˝ÇĆĆ˝â°ć, REFER TO WWW.şŁ˝ÇĆĆ˝â°ć.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 şŁ˝ÇĆĆ˝â°ć, REFER TO WWW.şŁ˝ÇĆĆ˝â°ć.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
