PneumaCult™-ALI Medium for Airway Epithelial Cell Culture

PneumaCult™-ALI Medium

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

Skip to the beginning of the images gallery

Need robust HAECs for differentiation? Begin your workflow by expanding HAECs in PneumaCult™-NGEx Medium for optimal ALI cultures.

PneumaCult™-ALI Medium

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

Format

Size

1 Kit Request Pricing

Catalog #

(Select a product)

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

Request Pricing Request Pricing

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

Request Pricing

Thank you for your interest in this product. Please provide us with your contact information and your local representative will contact you with a customized quote. Where appropriate, they can also assist you with a(n):

Estimated delivery time for your area

Product sample or exclusive offer

In-lab demonstration

By submitting this form, you are providing your consent to ��ƽ�� Technologies Canada Inc. and its subsidiaries and affiliates (“��ƽ��”) to collect and use your information, and send you newsletters and emails in accordance with our privacy policy. Please contact us with any questions that you may have. You can unsubscribe or change your email preferences at any time.

This site is protected by reCAPTCHA and the ��Ի��.

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
Heparin Solution
Cell culture supplement
PneumaCult™-NGEx Medium
Serum- and BPE-free culture medium for the expansion of human large airway, small airway, and nasal epithelial cells
Labeling Antibodies
Compatible antibodies for purity assessment of isolated cells

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™-NGEx Medium (Catalog #100-1505) 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™.

For information about introductory offers to try PneumaCult™ in your lab, fill out this form.

Specialized Media

Airway Cells

Human

Cell Culture, Differentiation, Maintenance, Organoid Culture

PneumaCult

Disease Modeling, Drug Discovery and Toxicity Testing, Epithelial Cell Biology

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

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 Name

Catalog #

05001

Lot #

All

Language

English

Document Type

Product Name

Catalog #

05021

Lot #

All

Language

English

Document Type

Product Name

Catalog #

05022

Lot #

All

Language

English

Document Type

Product Name

Catalog #

05001

Lot #

All

Language

English

Document Type

Product Name

Catalog #

05001

Lot #

All

Language

English

Document Type

Product Name

Catalog #

05001

Lot #

All

Language

English

Document Type

Product Name

Catalog #

05021

Lot #

All

Language

English

Document Type

Product Name

Catalog #

05021

Lot #

All

Language

English

Document Type

Product Name

Catalog #

05021

Lot #

All

Language

English

Document Type

Product Name

Catalog #

05022

Lot #

All

Language

English

Document Type

Product Name

Catalog #

05022

Lot #

All

Language

English

Document Type

Product Name

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

Workflow Stages for Airway Epithelial Cell Research

Expansion

Differentiation

Resources and Publications

Evolutionary loss of an antibiotic efflux pump increases Pseudomonas aeruginosa quorum sensing mediated virulence in vivo S. E. Fernandes et al. 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

Elexacaftor/Tezacaftor/Ivacaftor Supports Treatment for CF with ΔI1023-V1024-CFTR Y. Huang et al. International Journal of Molecular Sciences 2025 May

Abstract

Cystic Fibrosis (CF) is a common genetic disease in the United States, resulting from mutations in the Cystic Fibrosis transmembrane conductance regulator (cftr) gene. CFTR modulators, particularly Elexacaftor/Tezacaftor/Ivacaftor (ETI), have significantly improved clinical outcomes for patients with CF. However, many CFTR mutations are not eligible for CFTR modulator therapy due to their rarity. In this study, we report that a patient carrying rare complex CFTR mutations, c.1680-877G>T and c.3067_3072delATAGTG, showed positive clinical outcomes after ETI treatment. We demonstrate that ETI was able to increase the expression of CFTR harboring c.3067_3072delATAGTG in a heterologous system. Importantly, patient-derived nasal epithelial cells in an air–liquid interface (ALI) culture showed improved CFTR function following ETI treatment. These findings supported the initiation of ETI with the patient. Retrospective studies have suggested that the patient has shown small but steady improvement over the past two years in several clinical metrics, including lung function, body mass index (BMI), and sweat chloride levels. Our studies suggest that ETI could be beneficial for patients carrying c.3067_3072delATAGTG.

mTOR inhibition impacts the flagellin-augmented inflammatory and antimicrobial response of human airway epithelial cells to Pseudomonas aeruginosa C. C. V. Linge et al. PLOS One 2025 May

Abstract

The airway epithelium provides a first line of defense against pathogens by release of antimicrobial factors and neutrophil-attracting chemokines. Pseudomonas (P.) aeruginosa , a Gram-negative bacterium that expresses flagellin as an important virulence factor, is a common cause of injurious airway inflammation. The aim of our study was to determine the contribution of flagellin to the inflammatory, antimicrobial, and metabolic responses of the airway epithelium to P. aeruginosa . Furthermore, as we previously showed that targeting mTOR limited the glycolytic and inflammatory response induced by flagellin, we assessed the effect of rapamycin on human bronchial epithelial (HBE) cells stimulated with flagellated and non-flagellated P. aeruginosa. Primary pseudostratified HBE cells, cultured on an air-liquid-interface, were treated on the basolateral side with medium, vehicle or rapamycin, exposed on the apical side with flagellated or flagellin-deficient P. aeruginosa , and analyzed for their inflammatory, antimicrobial, and glycolytic responses. Flagellin augmented the P. aeruginosa -induced expression of antimicrobial factors and secretion of chemokines by HBE cells but did not further increase the glycolytic response. Treatment of HBE cells with rapamycin inhibited mTOR activation in general and flagellin-augmented mTOR activation in particular, but did not affect the glycolytic response. Rapamycin, however, diminished the flagellin-augmented inflammatory and antimicrobial response induced by Pseudomonas . These results demonstrate that flagellin is a significant factor that augments the inflammatory and antimicrobial response of human airway epithelial cells upon exposure to P. aeruginosa and suggest that mTOR inhibition by rapamycin in the airway epithelium diminishes these exaggerated responses.

View All Publications

Related Products

Need robust HAECs for differentiation? Begin your workflow by expanding HAECs in PneumaCult™-NGEx Medium for optimal ALI cultures.

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 ��ƽ��, REFER TO WWW.��ƽ��.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

�����ƽ��

PneumaCult™-ALI Medium

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

PneumaCult™-ALI Medium

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

Product Advantages

What's Included

Request Pricing

Overview

More Information

Data Figures

Protocols and Documentation

Applications

Resources and Publications

Educational Materials (24)

Publications (121)

Abstract

Abstract

Abstract

Related Products

Item added to your cart

��ƽ��