This photomicrograph depicts airway epithelial cells from lung tissue of a COPD patient. The cell nuclei have been stained to reveal IL-33, a type of signaling molecule found at high levels in COPD patients. New research shows that viral infection can induce these cells to proliferate. Release of IL-33 from these cells promotes inflammatory mucus production. These findings provide insight into the mechanisms linking acute infection to chronic inflammatory lung disease. (Source: Holtzman Lab)This photomicrograph depicts airway epithelial cells from lung tissue of a COPD patient. The cell nuclei have been stained to reveal IL-33, a type of signaling molecule found at high levels in COPD patients. New research shows that viral infection can induce these cells to proliferate. Release of IL-33 from these cells promotes inflammatory mucus production. These findings provide insight into the mechanisms linking acute infection to chronic inflammatory lung disease. (Source: Holtzman Lab)
Thu, 08/15/2013 - 2:23pm


Investigators at Washington University School of Medicine in St. Louis have described another link in the chain of events that connect acute viral infections to the development of chronic obstructive pulmonary disease (COPD). Their discovery points to a new therapeutic target for COPD, an extremely common disease of the lower airways that is seen in chronic bronchitis and emphysema.
COPD affects about 12 million people in the United States, where it is the third leading cause of death. Worldwide, it is the fifth leading cause of death. It is characterized by inflammation of the lower airways and destruction of lung tissue that limit airflow and pulmonary function. No effective treatments exist to specifically address a major cause of disease advancement and death from COPD – excess inflammatory mucus that blocks airways and prevents normal breathing.
It is well established that smoke exposure is a major risk factor for COPD, but in this new research, investigators show that the cells that line the airways also can respond to viruses in a way that leads to long-term lung inflammation and mucus production that are typical of COPD.
The research, featured on the cover of the September issue of the Journal of Clinical Investigation, reconciles the discrepancy between the transient nature of most viral infections and the relatively permanent nature of chronic inflammatory diseases such as COPD.
Michael J. Holtzman, MD, the Selma and Herman Seldin Professor of Medicine at Washington University, has devoted much of his career to understanding the connections between environmental agents and development of chronic lung disease. Five years ago, he and his colleagues reported that a signaling molecule called interleukin-13 (IL-13) was the key driver of excess production of chronic airway mucus after viral infection. Since then, they have pursued the basis for IL-13 production and its usefulness as a marker and a target for more precise therapeutic intervention in COPD and related diseases such as asthma.

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