( Enlisted to help fight viral infections...)Shorter colds, milder flu may follow from newly revealed immune mechanism

Enlisted to help fight viral infections, immune cells called macrophages consume virus-infected cells to stop the spread of the disease in the body. Now researchers at Washington University School of Medicine in St. Louis have uncovered how macrophages keep from succumbing to the infection themselves. Boosting this mechanism may be a way to speed recovery from respiratory infections.

The researchers found that a specific protein produced in the course of respiratory viral infections can serve to protect macrophages from an untimely death. Their report will appear in an upcoming issue of Nature Medicine and is available on October 9 at the journal's website.

"If the macrophages were to die, the infection would spread further," says senior author Michael J. Holtzman, M.D., the Selma and Herman Seldin Professor of Medicine and director of pulmonary and critical care medicine. "So the macrophages use a protein called CCL5 to ensure that the infection process can be stopped before it goes any further."

Holtzman thinks the information about the role of CCL5 may lead to new methods to hasten recovery from respiratory viral inflections like influenza or the common cold, which at present have no pharmacological cure.

CCL5's role was discovered while Holtzman's group was testing mice that had respiratory infections. They found that the sick mice produced massive amounts of CCL5--about a hundred times more than they produced when healthy.

"CCL5 was just off the chart compared to the other 30,000 mouse genes," Holtzman says. "Then the challenge was to figure out why CCL5 gene expression should be so far above everything else."

They found that mice lacking the gene to make CCL5 died much more frequently from respiratory virus infection than normal mice. Examining lung tissues from these CCL5-deficient mice, the researchers saw that macrophages--which would ordinarily enter the airway, clean up virus-infected cells and then leave--
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Source:Washington University School of Medicine

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