02/01/07
New research suggests that different treatments may be needed for chronic asthma, depending on whether it results from allergies or lung infections.
Previous studies have shown that certain lung infections such as Mycoplasma pneumoniae can linger on and contribute to a person later experiencing symptoms of asthma.
Researchers at UT Southwestern have now identified a particular gene that influences how severe a M. pneumoniae infection can be, which in turn suggests that a different strategy might be needed for treating asthma resulting from this and similar lung infections rather than allergies.
“What this shows is that infectious asthma might have a different mechanism than allergic asthma. Most people think asthma is asthma, but it may be multifaceted,” said Robert Hardy, MD, an infectious disease specialist at UT Southwestern.
That’s an important implication because the latest statistics show that asthma is on the rise. According to the US Centers for Disease Control, more than 20 million Americans currently have asthma and another 10 million have been diagnosed with asthma at some point in their life. Roughly 6.5 million American children, or nearly 9% of the nation’s pre-adult population, have asthma, figures released in December show.
Hardy, an assistant professor of internal medicine and pediatrics at UT Southwestern, has been using mice to study how certain pneumonia bacteria contribute to chronic asthma and, in this latest study, identified how a particular gene might contribute to more severe lung infection. The research appears in the January edition of Infection and Immunity.
To investigate the mechanism by which M. pneumoniae causes lung disease and respiratory difficulties, the UT Southwestern researchers inoculated two different types of mice with this bacterium. The study contrasted the reaction of one normal group of mice with another group lacking a particular gene called IL-12, which is involved in immune response. The mice engineered without the gene showed significantly less lung inflammation than the mice that naturally had the gene, with some indicators showing seven times less inflammation.
“M. pneumoniae might be more of a cofactor in developing chronic asthma than a direct cause, similar to how high cholesterol or diabetes makes people more vulnerable to heart attacks,” Hardy said, pointing to a number of previous studies. “It’s probably not the only thing, but it’s one of them. In some people it might incite asthma or it might exacerbate it.”
