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TRPA1: Better Target for CF Therapy?

November 10, 2016 at 2:22 pm

By Paul Schumacker, PhD, editor, American Journal of Respiratory Cell and Molecular Biology

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Transient Receptor Potential Ankyrin1 Channels Modulate Inflammatory Response in Respiratory Cells from Patients with Cystic Fibrosis

Currently available drugs reduce the lung tissue damage caused by the recurrent bacterial infections and inflammatory responses in patients with cystic fibrosis, but the drugs’ efficacy is limited and not without side effects. In their November  American Journal of Respiratory Cell and Molecular Biology article, Paola Prandini and colleagues report findings of an in vitro study to determine if Transient Receptor Potential Ankyrin 1 (TRPA1) calcium channels would be a better therapeutic target. They found that inhibition of TRPA1 expression reduces release of several cytokines in CF epithelial cells exposed to Pseudomonas aeruginosa infection, suggesting these channels may be a target for drugs that could reduce tissue damage “without completely blunting the immune response.”

November Highlights

Role of Twist1 Phosphorylation in Angiogenesis and Pulmonary Fibrosis

IL-13+ Type 2 Innate Lymphoid Cells Correlate with Asthma Control Status and Treatment Response

IL-23 Is Essential for the Development of Elastase-Induced Pulmonary Inflammation and Emphysema

Parenchymal Airspace Profiling: Sensitive Quantification and Characterization of Lung Structure Evaluating Parenchymal Destruction

Functional Characterization of ATP-Binding Cassette Transporter A3 Gene Mutations from Infants with Respiratory Distress Syndrome

Functional Toll-Like Receptor 9 Expression and CXCR3 Ligand Release in Pulmonary Sarcoidosis


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