PneumaCult™-ALI Medium
Serum- and BPE-free medium for human airway epithelial cells cultured at the air-liquid interface
Need robust HAECs for differentiation? Begin your workflow by expanding HAECs in PneumaCult™-NGEx Medium for optimal ALI cultures.
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- PneumaCult™-NGEx Medium
Serum- and BPE-free culture medium for the expansion of human large airway, small airway, and nasal epithelial cells
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Find supporting information and directions for use in the Product Information Sheet or explore additional protocols below.
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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 (26)
Publications (124)
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.
Innate airway responses shape permissiveness to human respiratory syncytial virus
Virus Research 2026 Apr
Abstract
The interaction between human respiratory syncytial virus (HRSV) and the innate immune system has been demonstrated both in vitro and in vivo. Disruption of interferon (IFN) signaling pathways increases susceptibility and permissiveness to HRSV infection, whereas pretreatment of cells with IFN confers (partial) resistance. This suggests that HRSV disease severity is likely influenced by a pre-existing antiviral state of the respiratory epithelium, driven by baseline or primed expression of type I and type III IFNs. Here, we investigated whether prior exposure to respiratory bacteria or viruses alters in vitro susceptibility and permissiveness to HRSV infection by shaping an antiviral state using both immortalized cell lines and airway organoid models. In A549 cells, pre-exposure to S. aureus had the most significant impact by reducing HRSV infection and inducing robust interferon responses. However, this effect was not reproduced in airway organoids. Conversely, sequential virus infection experiments in airway organoids revealed that prior infection with human parainfluenza virus type 3 (HPIV‑3) reduced the spread of subsequent HRSV infection. In addition to interferon signaling this proved to be associated with epithelial damage mediated by HPIV-3 infection. Collectively, these findings show that HRSV susceptibility and permissiveness are influenced by the up- or downregulation of specific anti- and pro-viral factors induced by prior bacterial or viral exposure, together with the maintenance or disruption of epithelial integrity. Understanding these interactions could be crucial when identifying specific risk groups for severe HRSV-associated disease and the development of targeted HRSV interventions.
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
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Need robust HAECs for differentiation? Begin your workflow by expanding HAECs in PneumaCult™-NGEx Medium for optimal ALI cultures.
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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 chemicals including Nickel Compounds which are known to the State of California to cause cancer and birth defects or other reproductive harm. For more information go to
