Investigators Reveal a Key to Virus-Induced Asthma
Asthma and Virus
Researchers have discovered a new way to distinguish virus-induced asthma from that of allergen-caused disease based on a study of 59 asthma patients who were experiencing an acute asthma exacerbation.
Writing in the second issue for August 2005 of the American Journal of Respiratory and Critical Care Medicine, Peter G. Gibson, M.B.B.S., of the JohnHunterHospital in New Lambton, New South Wales, Australia, along with seven associates, compared the sputum cellular profiles of the 59 acute asthmatics against those of 45 controls. The control group included 14 patients with stable asthma and no viral infection, 15 subjects without asthma but with a viral infection and 16 healthy, uninfected persons. To establish infection status and pulmonary status/history, participants completed common cold and asthma questionnaires, microbiological tests, and lung function and allergy (atopy) tests.
"A respiratory virus was detected in 46, or 78 percent, of the subjects with acute asthma," said Dr. Gibson.
Asthma exacerbations are caused by viral respiratory infections in both children and adults. Specific viruses detected among the acute asthma patients in this study included rhinovirus (83 percent of the cases), influenza, enterovirus and respiratory syncytial virus. In addition, however, the researchers found interleukin 1 (IL-10) to be another major factor involved in the acute asthma exacerbations of those with respiratory infections.
"IL-10 gene expression was significantly increased in acute asthma with virus infection when compared with virus infection controls, uninfected controls and subjects with stable asthma," said Dr. Gibson.
He noted that, upon recovery from acute asthma, IL-10 gene expression, which functions as a potent immunoregulator to suppress immune responses broadly, returned to normal levels.
"Thus, IL-10 gene expression from airway cells appeared to be a feature of virus-induced acute asthma," said Dr. Gibson.
The researchers also pointed out that in other studies, viral infection had been reported to increase IL-10 protein levels in the nose and in peripheral blood mononuclear cells.
After describing the gene expression and cellular profiles of these patients, they reported that the results show that in virus-induced asthma, there are different mechanisms operating than those described in allergen-induced asthma.
In an editorial on the article, William W. Busse, M. D., and James E. Gern, M.D., of the University of Wisconsin Hospital in Madison, wrote: "The observations of the author and his colleagues point to IL-10 as an indicator of rhinovirus-provoked asthma, both in children and adults. This, by itself, is a major step forward in identifying the key players in virus-provoked asthma. Many additional pieces, such as in the following, need to be placed in the puzzle to more fully understand how respiratory viruses induce an asthma exacerbation: (1) host susceptibility factors, (2) mechanisms of the acute and often unresponsive airflow obstruction, and (3) effective treatment for both intervention and prevention. The observations by the authors add critical new information as we try to understand the mystery of how an innocuous respiratory infection, like the common cold, produced by rhinovirus, can have such devastating effects in some patients with asthma."