New drugs can limit mucus production to treat asthma and COPD
Respiratory diseases such as asthma and chronic obstructive pulmonary disease (COPD) are one of the common causes of death worldwide, but there has been no effective treatment to solve the main cause of death-excessive production of mucus.
Michael J. Holtzman, a medical professor at Washington University School of Medicine in St. Louis, said: There is good evidence that the main cause of death from severe chronic obstructive pulmonary disease or asthma is airway mucus obstruction.
Now, Holtzman and his colleagues have clarified the molecular pathway responsible for the production of excess mucus in airway cells, and using this information, a series of new drugs have been designed to suppress this pathway.
Their findings were published in the Journal of Clinical Investigation on November 26.
In the United States and around the world, chronic respiratory diseases, especially chronic obstructive pulmonary disease, are the third leading cause of death. Smoking and exposure to pollution are the main causes of these diseases. Morbidity and mortality are closely linked. Too much mucus blocking the airway inhibits normal breathing. However, there is no effective treatment to suppress the excess production of respiratory mucus.
In the new study, scientists discovered that an important signaling molecule CLCA1 has a special role in the mucus production pathway. They showed that CLCA1 allows IL-13 protein to turn on the expression of major mucus genes in airway cells. The researchers also found that CLCA1 needs the help of the enzyme MAPK13.
Although there is no existing drug that acts on MAPK13, Holtzman said that there are several compounds that can inhibit the enzyme MAPK14. We can use MAPK14 inhibitors to design new drugs that bind to specific activity pockets of MAPK14 to prevent its activity. The active pocket of MAPK13 itself has certain obstacles, and the spatial structure is becoming more and more crowded, so these old drugs cannot enter the protein active pocket.
Therefore, Holtzman and his team designed a slim structure drug that can avoid obstacles and better adapt to the pocket that binds MAPK13 protein.
The newly designed drugs can better bind to the MAPK13 pocket. In fact, the results show that some newly designed MAPK13 inhibitors reduce the production of cultured human respiratory tract cell mucus by up to 100 times.
But this research work must be carried out in human cells, because commonly used laboratory animals have different ways of producing mucus. For example, MAPK13 inhibitors are not effective in mice because other types of CLCA and MAPK proteins can continue to produce excess mucus. In addition to chronic obstructive pulmonary disease and asthma, Holtzman has also seen that MAPK13 inhibitors may also play a role in diseases with excessive mucus symptoms such as cystic fibrosis and even the common cold.
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