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PneumaCult™-ALI Medium

Serum- and BPE-free medium for human airway epithelial cells cultured at the air-liquid interface

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PneumaCult™-ALI Medium

Serum- and BPE-free medium for human airway epithelial cells cultured at the air-liquid interface

From: 296 USD
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Serum- and BPE-free medium for human airway epithelial cells cultured at the air-liquid interface
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Product Advantages


  • HBECs cultured with PneumaCult™-ALI undergo extensive mucociliary differentiation to form a pseudostratified epithelium that closely resembles the human airway

  • PneumaCult™-ALI is serum-free and BPE-free to minimize variability

What's Included

  • PneumaCult™-ALI Basal Medium, 450 mL
  • PneumaCult™-ALI 10X Supplement, 50 mL
  • PneumaCult™-ALI Maintenance Supplement (100X), 5 x 1 mL
Products for Your Protocol
To see all required products for your protocol, please consult the Protocols and Documentation.
  1. PneumaCult™-Ex Plus Medium
    PneumaCult™-Ex Plus Medium

    Serum- and BPE-free medium for expansion of primary human airway epithelial cells

  2. Animal Component-Free Cell Dissociation Kit
    Animal Component-Free Cell Dissociation Kit

    Dissociation kit for human stem and progenitor cells

  3. Hydrocortisone Stock Solution
    Hydrocortisone Stock Solution

    Cell culture supplement

  4. Heparin Solution
    Heparin Solution

    Cell culture supplement

Overview

PneumaCult™-ALI Medium (Catalog #05001) is a serum- and BPE-free medium for the culture of human airway epithelial cells at the air-liquid interface (ALI). Airway epithelial cells cultured in PneumaCult™-ALI Medium undergo extensive mucociliary differentiation to form a pseudostratified epithelium that exhibits morphological and functional characteristics similar to those of the human airway in vivo. PneumaCult™-ALI Medium is also available in a kit that includes 12 mm Transwell® inserts (Catalog #05021) or 6.5 mm Transwell® inserts (Catalog #05022).

Together, PneumaCult™-ALI Medium and PneumaCult™-Ex Plus Medium (Catalog #05040) constitute a fully integrated BPE-free culture system for in vitro human airway modeling that is also compatible with primary human nasal epithelial cells. This robust and defined system is a valuable tool for basic respiratory research, toxicity studies, and drug development.

Learn how to culture human airway epithelial cells at the ALI in our On-Demand Pulmonary Course or browse our Frequently Asked Questions (FAQs) about the ALI culture workflow using PneumaCult™.
Subtype
Specialized Media
Cell Type
Airway Cells
Species
Human
Application
Cell Culture, Differentiation, Maintenance, Organoid Culture
Brand
PneumaCult
Area of Interest
Disease Modeling, Drug Discovery and Toxicity Testing, Epithelial Cell Biology
Formulation Category
Serum-Free

More Information

More Information
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 www.P65Warnings.ca.gov

Data Figures

Figure 1. Overview of the PneumaCult™ Culture System

Expansion of human bronchial epithelial cells (HBECs) in submerged culture is performed with PneumaCult™-Ex Plus or PneumaCult™-Ex. During the early Expansion Phase of the ALI culture procedure, PneumaCult™-Ex Plus or PneumaCult™-Ex is applied to the apical and basal chambers. Upon reaching confluence, the culture is air-lifted by removing the culture medium from both chambers, and adding PneumaCult™-ALI to the basal chamber only. Differentiation into a pseudostratified mucociliary epithelium is obtained following 21-28 days of incubation and can be maintained for more than one year.

Figure 2. HBECs Cultured in PneumaCult™-Ex Successfully Differentiate into a Pseudostratified Mucociliary Epithelium with PneumaCult™-ALI

Early-passage (P1-3) HBECs cultured in PneumaCult™-Ex successfully differentiate when cultured at air-liquid interface with PneumaCult™-ALI for 28 days. H&E staining revealed the pseudostratifi ed structure of the epithelium with cilia present at the apical surface (A). Periodic acid-Schiff staining demonstrated the presence of goblet cells (B). The presence of ciliated and goblet cells was also demonstrated by immunofl uorescence staining of cilia marker acetylated (AC)-Tubulin (green; C) and the goblet cell marker Mucin5AC (green; D). Appropriate positioning of basal cells along the transwell insert was visualized by immunofl uorescence staining using the basal cell markers p75NTR (green) and p63 (red; E,F). A representative merged image indicates the apical cells, detected by DAPI alone, positioned along the epithelium and in close contact with the basal cells (detected by DAPI, p63 and p75NTR co-labeling) located along the insert (G).

Figure 3. Electrophysiological characterization of differentiated HBECs (P4) that were expanded in PneumaCult™-Ex Plus, PneumaCult™-Ex, and Bronchial Epithelial Growth Media

TEER (A) and representative characterization of the ion channel activities (B) for ALI cultures at 28 days post air-lift using HBECs expanded in PneumaCult™-Ex Plus, PneumaCult™-Ex, or Bronchial Epithelial Growth Media. Amiloride: ENaC inhibitor. IBMX and Forskolin: CFTR activators. Genistein: CFTR potentiator. CFTRinh-172: CFTR inhibitor. UTP: Calciumactivated Chloride channels (CaCCs) activator. All ALI differentiation cultures were performed using PneumaCult™-ALI.

Protocols and Documentation

Find supporting information and directions for use in the Product Information Sheet or explore additional protocols below.

Document Type
Product Name
Catalog #
Lot #
Language
Document Type
Product Information Sheet
Product Name
PneumaCult™-ALI Medium
Catalog #
05001
Lot #
All
Language
English
Document Type
Product Information Sheet
Product Name
PneumaCult™-ALI Medium with 12 mm Transwell® Inserts
Catalog #
05021
Lot #
All
Language
English
Document Type
Product Information Sheet
Product Name
PneumaCult™-ALI Medium with 6.5 mm Transwell® Inserts
Catalog #
05022
Lot #
All
Language
English
Document Type
Safety Data Sheet 1
Product Name
PneumaCult™-ALI Medium
Catalog #
05001
Lot #
All
Language
English
Document Type
Safety Data Sheet 2
Product Name
PneumaCult™-ALI Medium
Catalog #
05001
Lot #
All
Language
English
Document Type
Safety Data Sheet 3
Product Name
PneumaCult™-ALI Medium
Catalog #
05001
Lot #
All
Language
English
Document Type
Safety Data Sheet 1
Product Name
PneumaCult™-ALI Medium with 12 mm Transwell® Inserts
Catalog #
05021
Lot #
All
Language
English
Document Type
Safety Data Sheet 2
Product Name
PneumaCult™-ALI Medium with 12 mm Transwell® Inserts
Catalog #
05021
Lot #
All
Language
English
Document Type
Safety Data Sheet 3
Product Name
PneumaCult™-ALI Medium with 12 mm Transwell® Inserts
Catalog #
05021
Lot #
All
Language
English
Document Type
Safety Data Sheet 1
Product Name
PneumaCult™-ALI Medium with 6.5 mm Transwell® Inserts
Catalog #
05022
Lot #
All
Language
English
Document Type
Safety Data Sheet 2
Product Name
PneumaCult™-ALI Medium with 6.5 mm Transwell® Inserts
Catalog #
05022
Lot #
All
Language
English
Document Type
Safety Data Sheet 3
Product Name
PneumaCult™-ALI Medium with 6.5 mm Transwell® Inserts
Catalog #
05022
Lot #
All
Language
English

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.

Research Area
Workflow Stages

Resources and Publications

Educational Materials (24)

Modeling Cystic Fibrosis Airway: PneumaCult™-Ex Plus and PneumaCult™-ALI
Brochure
Modeling Cystic Fibrosis Airway: PneumaCult™-Ex Plus and PneumaCult™-ALI
Pulmonary Research
Brochure
Pulmonary Research
Air-Liquid Interface Culture for Respiratory Research
Technical Bulletin
Air-Liquid Interface Culture for Respiratory Research
How to Process Epithelial Organoids and Organoid-Derived Epithelial Monolayers for RNA Isolation
Protocol
How to Process Epithelial Organoids and Organoid-Derived Epithelial Monolayers for RNA Isolation
How to Co-Culture Human Airway Epithelial and Immune Cells for RSV Infection
Protocol
How to Co-Culture Human Airway Epithelial and Immune Cells for RSV Infection
How to Perform Immunocytochemistry (ICC) Staining of Epithelial Cells Cultured as Monolayers or at the Air-Liquid Interface
Protocol
How to Perform Immunocytochemistry (ICC) Staining of Epithelial Cells Cultured as Monolayers or at t...
How to Perform a TEER Measurement to Evaluate Epithelial Barrier Integrity in ALI Cultures
4:25
Video
How to Perform a TEER Measurement to Evaluate Epithelial Barrier Integrity in ALI Cultures
How to Model the Human Airway at the Air-Liquid Interface: Expansion of HBECs
7:42
Video
How to Model the Human Airway at the Air-Liquid Interface: Expansion of HBECs
Air-Liquid Interface (ALI) Culture of Bronchial Epithelial Cells with PneumaCult™-ALI Medium
2:01
Video
Air-Liquid Interface (ALI) Culture of Bronchial Epithelial Cells with PneumaCult™-ALI Medium
Correlating TEER Values with Air-Liquid Interface Culture Morphology
3:02
Video
Correlating TEER Values with Air-Liquid Interface Culture Morphology
How to Model the Human Airway at the Air-Liquid Interface: Differentiation of HBECs
5:03
Video
How to Model the Human Airway at the Air-Liquid Interface: Differentiation of HBECs
Beating Cilia of ALI Cultures Grown in PneumaCult™
0:31
Video
Beating Cilia of ALI Cultures Grown in PneumaCult™
Why Use Air-Liquid Interface Cultures for Respiratory Research: Q&A with Dr. Wadsworth
3:55
Video
Why Use Air-Liquid Interface Cultures for Respiratory Research: Q&A with Dr. Wadsworth
How to Model the Human Airway at the Air-Liquid Interface: Introduction
2:13
Video
How to Model the Human Airway at the Air-Liquid Interface: Introduction
Thinking Outside the Dome: Versatile Organotypic Cell Culture Methods
39:57
Webinar
Thinking Outside the Dome: Versatile Organotypic Cell Culture Methods
PneumaCult™-ALI: An Improved Medium Formulation for the Differentiation of Human Bronchial Epithelial Cells
47:25
Webinar
PneumaCult™-ALI: An Improved Medium Formulation for the Differentiation of Human Bronchial Epithel...
Studying Respiratory Viruses with ALI Cultures
6:56
Webinar
Studying Respiratory Viruses with ALI Cultures
Studying Cystic Fibrosis Using Primary Human Nasal Epithelial Cells
51:30
Webinar
Studying Cystic Fibrosis Using Primary Human Nasal Epithelial Cells
Organoid Expert Panel
52:35
Webinar
Organoid Expert Panel
In Vitro Human Airway Modeling Using Primary Airway Epithelial Cells
18:41
Webinar
In Vitro Human Airway Modeling Using Primary Airway Epithelial Cells
Airway Epithelial Cells of the Human Respiratory System
Mini Review
Airway Epithelial Cells of the Human Respiratory System
PneumaCult™: an Integrated Culture Medium System for in Vitro Human Airway Modeling
Scientific Poster
PneumaCult™: an Integrated Culture Medium System for in Vitro Human Airway Modeling
Generation of Fully Differentiated and Functional Human Small Airway Cultures
Scientific Poster
Generation of Fully Differentiated and Functional Human Small Airway Cultures
Pulmonary Course
On-Demand Training
Pulmonary Course

Publications (98)

Functional rescue of c.3846G\textgreaterA (W1282X) in patient-derived nasal cultures achieved by inhibition of nonsense mediated decay and protein modulators with complementary mechanisms of action. O. Laselva et al. Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society 2020 sep

Abstract

BACKGROUND The nonsense mutation, c.3846G{\textgreater}A (aka: W1282X-CFTR) leads to a truncated transcript that is susceptible to nonsense-mediated decay (NMD) and produces a shorter protein that is unstable and lacks normal channel activity in patient-derived tissues. However, if overexpressed in a heterologous expression system, the truncated mutant protein has been shown to mediate CFTR channel function following the addition of potentiators. In this study, we asked if a quadruple combination of small molecules that together inhibit nonsense mediated decay, stabilize both halves of the mutant protein and potentiate CFTR channel activity could rescue the functional expression of W1282X-CFTR in patient derived nasal cultures. METHODS We identified the CFTR domains stabilized by corrector compounds supplied from AbbVie using a fragment based, biochemical approach. Rescue of the channel function of W1282X.-CFTR protein by NMD inhibition and small molecule protein modulators was studied using a bronchial cell line engineered to express W1282X and in primary nasal epithelial cultures derived from four patients homozygous for this mutation. RESULTS We confirmed previous studies showing that inhibition of NMD using the inhibitor: SMG1i, led to an increased abundance of the shorter transcript in a bronchial cell line. Interestingly, on top of SMG1i, treatment with a combination of two new correctors developed by Galapagos/AbbVie (AC1 and AC2-2, separately targeting either the first or second half of CFTR and promoting assembly, significantly increased the potentiated channel activity by the mutant in the bronchial epithelial cell line and in patient-derived nasal epithelial cultures. The average rescue effect in primary cultures was approximately 50{\%} of the regulated chloride conductance measured in non-CF cultures. CONCLUSIONS These studies provide the first in-vitro evidence in patient derived airway cultures that the functional defects incurred by W1282X, has the potential to be effectively repaired pharmacologically.
Ionocytes and CFTR Chloride Channel Expression in Normal and Cystic Fibrosis Nasal and Bronchial Epithelial Cells. P. Scudieri et al. Cells 2020 sep

Abstract

The airway epithelium contains ionocytes, a rare cell type with high expression of Forkhead Box I1 (FOXI1) transcription factor and Cystic Fibrosis Transmembrane conductance Regulator (CFTR), a chloride channel that is defective in cystic fibrosis (CF). Our aim was to verify if ionocyte development is altered in CF and to investigate the relationship between ionocytes and CFTR-dependent chloride secretion. We collected nasal cells by brushing to determine ionocyte abundance. Nasal and bronchial cells were also expanded in vitro and reprogrammed to differentiated epithelia for morphological and functional studies. We found a relatively high ({\~{}}3{\%}) ionocyte abundance in ex vivo nasal samples, with no difference between CF and control individuals. In bronchi, ionocytes instead appeared very rarely as previously reported, thus suggesting a possible proximal-distal gradient in human airways. The difference between nasal and bronchial epithelial cells was maintained in culture, which suggests an epigenetic control of ionocyte development. In the differentiation phase of the culture procedure, we used two media that resulted in a different pattern of CFTR expression: confined to ionocytes or more broadly expressed. CFTR function was similar in both conditions, thus indicating that chloride secretion equally occurs irrespective of CFTR expression pattern.
Interleukin 13 (IL-13) alters hypoxia-associated genes and upregulates CD73. S. M. Khalil et al. International forum of allergy {\&} rhinology 2020 sep

Abstract

BACKGROUND Interleukin 13 (IL-13) is a pleiotropic cytokine that has been shown to be important in the pathogenesis of chronic rhinosinusitis with nasal polyps (CRSwNP) and other type 2 inflammation-related diseases. Increased IL-13 expression can elicit several pro-inflammatory effects, including eosinophilia, and pathology such as increased mucus secretion. Polypogenesis in chronic rhinosinusitis (CRS) can be caused by hypoxia, which can also lead to hyperpermeability of airway epithelium and epithelium-to-mesenchymal translation through the upregulation of hypoxia-associated genes, such as HIF1. Whether T-helper 2 (Th2) inflammatory cytokines, such as IL-13, can also induce sinonasal epithelial hypoxia-associated genes is currently unknown. METHODS Human air-liquid interface (ALI) sinonasal epithelial cell cultures treated with recombinant IL-13 were analyzed by real-time polymerase chain reaction (PCR) and flow cytometry to determine the effect on epithelial cells. RESULTS Whole tissue from CRSwNP subjects showed increased HIF1A gene expression. Treatment of fully differentiated human ALI cultures with IL-13 resulted in a concurrent increase in HIF1A and ARNT messenger RNA (mRNA) expression. However, the level of EPAS1 expression was significantly reduced. IL-13 also had a dose-dependent response on the expression of HIF genes and the time course experiment showed peak expression of HIF1A and ARNT at 5 to 7 days poststimulation. Remarkably, CD73 surface expression also peaked at day 5 poststimulation. CONCLUSION Our data suggests that IL-13 can induce hypoxia signaling pathway genes leading to surface expression of CD73, which has an anti-inflammatory effect.
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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.

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 www.P65Warnings.ca.gov



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