Bolstering Alveolar Defense to Treat Complicated Influenza

Influenza is a major cause of global mortality and a frequent cause of pandemics, with death often resulting from secondary pneumonia by inhaled Staphylococcus aureus (SA), especially in children. New research is uncovering how influenza infection disrupts lung defenses and opens the door to deadly bacterial co-infections with SA.

Jaime Hook, MD, Assistant Professor, Division of Pulmonary, Critical Care, and Sleep Medicine, Departments of Medicine and Microbiology, Global Health and Emerging Pathogens Institute, Icahn School of Medicine at Mount Sinai, and her team are studying new therapeutic approaches for influenza lung infection that protect against fatal SA coinfection.

Hook spoke in the third issue of The Respiratory Report, a quarterly newsletter from HCPLive that is powered by the American Lung Association Research Institute, on her team’s current research in this area.

Her team found that influenza impairs alveolar defense by blocking CFTR-dependent liquid secretion and activating ENaC-driven absorption, creating an absorptive environment that allows inhaled Staphylococcus aureus to cause fatal lung injury and were able to rescue alveolar wall liquid secretion and protect against SA-induced lung injury with the CFTR potentiator drug ivacaftor.

"These findings support CFTR potentiator therapy as a new treatment strategy for flu, SA coinfection, and they also inform the design of new CFTR potentiating therapies that might have more precise alveolar sites of action, better drug efficacy, fewer side effects, and perhaps resilience in the face of new pandemic viruses and new viral and bacterial mutations that threaten the efficacy of existing drugs," Hook said.

To learn more about Hook's research, view the interview above or read her contribution to the third issue of The Respiratory Report here:

Developing new treatments for influenza that target the lung – not the virus