A new study could lead to therapeutic strategies for chronic lung disease

Scientists at the University of Washington School of Medicine in St. Louis have linked a type of immune cell in the development of a chronic lung disease that is sometimes triggered by a viral respiratory infection.

The evidence suggests that the activity of this immune cell – a type of immune cell called a dendritic cell – serves as an early turn that, when activated, triggers a series of events that trigger driving progressive lung disease, including asthma and chronic obstructive pulmonary disease (COPD).

The new study, published in The Journal of Ornithology, opens the door to potential prevention or treatment strategies for chronic lung disease. Immediately, by measuring the levels of these dendritic cells in clinical samples from patients hospitalized with a viral infection, such as influenza or COVID-19, doctors could help the patients. -patients at risk of respiratory failure and death.

Examining mice with respiratory viral infection that make the animals prone to developing malignant lung disease, the researchers showed that these dendritic cells communicate with the lining of the airway in ways which causes the air lining cells to grow up and the inflammatory symptoms.

The inflammation causes airway cells to grow beyond their normal limits and turn into cells that produce excess mucus and cause inflammation, which in itself causes coughing and respiratory difficulty.

We are trying to understand how a viral infection that appears to be cleared by the body nonetheless can promote chronic, progressive lung disease. Not everyone experiences this progress. We believe that there is a reversal, provoking the negative response. We recognize that inversion and ways to control it. This work tells us that this type of dendritic cell sits at that inversion stage. “

Michael J. Holtzman, MD, Senior Research Author, Selma and Herman Seldin Professor of Medicine, University of Washington School of Medicine

Holtzman ‘s work in the past has influenced the lining of the airway – where the viral infection takes hold – as the most likely cause of this process.

“But this study suggests the ban will start even further upstream,” said Holtzman, who is also director of the Department of Pulmonary and Critical Care Medicine. “Dendritic cells tell the cells lining the airway what to do. There is more work to be done, but these data tell us that dendritic cells play an important role in getting the net cells in the wrong direction. “

Holtzman calls this dendritic cell a type of sentinel because its job is to detect an invading virus and the body ‘s first immune response to the disease. The problem arises when the cell does not close properly after the threat has passed.

“Many people never develop chronic lung disease after a viral infection,” Holtzman said. “But others are genetically susceptible to this type of disease. People susceptible to viral infection include patients with asthma, COPD, and viral diseases such as COVID-19. It is essential to look for ways to fix this disease response and prevent the complications that can occur after the virus has gone away. “

In the meantime, Holtzman said, high levels of these dendritic cells and their results in hospitalized lung patients could warn doctors that such patients are prone to developing a serious disease and that between provide them with respiratory interventions and other supportive therapies that are tailored to their disease process.

“Similarly, if this process does not go ahead, the patient may be more likely to avoid these types of long-term complications,” Holtzman said. “We are following this line of research to help improve the prognosis of post-infection lung disease and to provide companion medications that can stop or reverse this change. to reverse the disease. “

Source:

Washington University School of Medicine

Magazine Reference:

Wang, X.,. et al. (2021) TLR3-Activated Dendritic Cells Dendritic Cells Progression from infectious disease to infectious disease of the lung. The Journal of Immunology. doi.org/10.4049/jimmunol.2000965.

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