Where do Human Airway Cells Come From?

Oxygenated air enters through the mouth or nose and passes into the trachea. The trachea branches into two bronchi, which lead to each lung. The bronchi divide into progressively smaller branches, called bronchioles. At the end of bronchioles are alveoli, sacs that mediate the exchange of oxygen and carbon dioxide.

A layer of epithelial cells lines the respiratory tract. This epithelium provides a barrier against the external environment and protects against infection from airborne pathogens. Defective barrier function or viral infection can lead to respiratory tract disease.

Studies Using Lifeline^® Airway Epithelial Cells

Tripathi et al. studied the antiviral activity of LL-37, a human antimicrobial peptide. They illustrated that LL-37 reduced the infective activity of a seasonal influenza strain, H3N2, but was not as effective against a pandemic strain, Cal09. Interestingly, when they tested the antiviral activity of LL-37 peptide derivatives, they found that a central fragment, GI-20, was effective against the seasonal H3N2 strain, as well as the pandemic Cal09 strain. The authors used Lifeline^® primary human bronchial tracheal epithelial cells (HBTE’s) and human small airway epithelial cells (HSAE’s) as host cells to test the activity of LL-37 and its derivatives against multiple strains of influenza virus. The results from this study suggest that LL-37 could be engineered to have increased antiviral activity as a defense against influenza.

Fu et al. investigated the cellular machinery that regulates the infectivity of the influenza A virus. They found that TRIM32, an E3 ubiquitin ligase, interacts with PB1, an essential subunit of the viral RNA polymerase complex that replicates influenza A viral genes to perpetuate infection. The authors demonstrate that TRIM32 ubiquitylates PB1 and targets it for proteasome-mediated degradation. This study utilized Lifeline^® primary human bronchial tracheal epithelial cells (HBTE’s), influenza A’s natural host cells, to measure the antiviral activity of TRIM32 after influenza A viral infection. The results of this study identify a cellular mechanism that regulates influenza A infectivity, and suggest that the TRIM32-mediated PB1 degradation pathway could be utilized to design therapeutic interventions against influenza infection.

Using Human Airway Cells in Research

Lifeline^® Human Airway Cells provide model systems to study:

• Pulmonary diseases such as asthma, COPD, cystic fibrosis, and lung cancer
• The effects of smoking on respiratory cell function
• Mechanisms of viral infection and cellular regulation of viral gene products

Lifeline^® offers a number of Human Airway Cell types and Optimized Cell Growth Media to assist your research, including:

• Bronchial/Tracheal Epithelial Cells
• Bronchial/Tracheal Smooth Muscle Cells
• Lung Small Airway Epithelial Cells
• Lung Fibroblasts
• Lung Smooth Muscle Cells
• Lobar Bronchial Epithelial Cells (Large Airway)

• BronchiaLife™ Epithelial Cell Culture Medium Complete Kit
• FibroLife^® S2 Complete Kit (for Human Lung Fibroblast Cell culture)
• VascuLife^® SMC Medium Complete Kit (for Bronchial/Tracheal Smooth Muscle Cells and Lung Smooth Muscle Cell culture)

Tell us how you are using Lifeline^® primary respiratory cells to answer your research questions!